Wardwise Treatment Guidelines

Wardwise Treatment Guidelines

Edited By :

Dr.Salim Al Mamun
MBBS(Raj);CCD(BIRDEM);
CMU(DU)
Medical officer
Tenglahata Uposhastha Kendro
Kazipur , Sirajganj.

drsalimalmamun@gmail.com
http://www.drsalimalmamun.wordpress.com
Management of some poisoning
Poisoning in Medicine Ward

1. Sedative poisoning
Diagnostic tools:
1. H/O of taking sedatives e.g. Sedil, lexotanil, Bopam etc.
2. Pt. may be disoriented or drowsy or in deep sleep.
3. Respiration is normal or depressed.
4. Planter reflex is normal or extensor.
5. Pupils mid dilated & sluggish reaction to light.
Management:
1. Diet- normal, plenty of tea, coffee by mouth if Pt. can swallow
2. NPO till recovery, If pt. is in deep sleep.
3. O2 inhalation 1-4 L/min, if respiration is depressed.
4. Infusion 5% DNS 1000 i/v @ 10 drops/ min.
5. Activated charcoal (Tab. Ultracarbon 2+2+2), if pt. present with in 1 hour.
6. Antidote of Benzodiazepine- Flumazenil, slowly IV, dose 0.2 mg over 30–60 seconds, repeated in 0.5 mg increments as needed up to a total dose of 3–5 mg.
Flumazenil is a benzodiazepine receptor-specific antagonist; it has no effect on ethanol, barbiturates, or other sedative-hypnotic agents.
Flumazenil should not be used in pt. with H/O seizures or in patients with preexisting seizure disorder, toxin induced cardio toxicity, co-ingestion with TCA. The duration of action of flumazenil is short (2–3 hours) and resedation may occur, requiring repeated doses.
Activated Charcoal: Activated charcoal effectively adsorbs almost all drugs and poisons. Poorly adsorbed substances include iron, lithium, potassium, sodium, mineral acids, and alcohols.
(Ref. CMDT 2010)
2. Tricyclic antidepressant poisoning (Tryptin)

Clinical features
1. H/O taking TCA drugs in over doses ie. Amitryptylin
2. Dilated pupil, ileus, and retention of urine.
3. Respiration may depressed.
4. Presence of arrhythmias in ECG may present
5. Hypotension may occur
6. Hyperreflexia with extensor plantar, coma, and seizures.
7. Improvement can be expected within 24 h.

Management
1. NPO till further order or recovery.
2. IV fluids infusion (5% DNS1000cc +5% DA1000cc i.v. @20 drops/min. stat & daily)
3. Gastric lavage may be given after delayed presentation.
4. Tab. Ultracarbon 2+2+2
5. Treatment of arrythmias
6. If convulsion present Diazepam and phenytoin.
7. ECG monitoring during the first 24 h and until ECG changes have disappeared for 12 h.
8. If acidosis present- IV sodibicarb
Note: Sodibicarb available at 7.5% 25 ml
Tips:
• Gastric elimination may be useful for 24 h after ingestion because tricyclics slow gastric emptying.
• Cardiac arrhythmias are more common if there is acidosis. Bicarbonate should be used to achieve an arterial pH of 7.5 urgently.
• If arrhythmias occur with no acidosis and fail to respond to treatment with amiodarone or phenytoin, bicarbonate (25-50 mL 8.4% IV) may still be useful with in 20 min.
• If VT compromising cardiac out put, Lidocaine 50-100mg i.v. should be given.
(Ref. Oxford American Hand book of critical care + Parvin Kumar & M. Clark)

3. Stupifying poisoning (unknown poisoning)
Diagnostic tools:
1. H/O of poisoning during traveling or ingestion or inhalation of foods or other substances by unknown person.
2. Pt. in deep sleep or drowsy
3. Pupil constricted or dilated and light reaction normal or absent
4. Circulation (Pulse & BP) usually normal
5. Respiration normal.
(Contradictory-in OPC poisoning pupil is constricted but bradycardia hypotension & crepitation present in lungs).

Management:
1. NPO till further order
2. Iv fluid Infusion
3. Inj. Omeprazole (40mg) 1 vial i/v slowly stat and daily
4. Continued catheterization (antibiotic if catheterization is done)
5. Monitor vital signs

(Ref. National guideline for management of poisoning)

4. Corrosive Poisoning (strong acid & alkali)
Management:
1. NPO TFO
2. Clearing of the airways
3. O2 inhalation 4-6 L/min
4. Irrigate exposed eyes with sterile cold water or saline at least for 20 minutes and continue until the pt. returns to normal
5. Infusion 5% DNS 1000 + 5% DA 1000 cc i/v @ 20 drops/ min.
6. Inj. Diclofen 1 amp. im stat. & SOS
7. Inj. Omeprazole 40 mg IV slowly stat. & B.D.

Tips:
1. Dilution or neutralization, induction of emesis, gastric aspiration and lavage are contra-indicated.
2. Emulcents- egg white, olive oil, butter, cold milk should be avoided.
3. As there is no specific antidote, symptomatic treatment is to be provided. Neutralization with alkali now a days is not done.
4. Surgical treatment must be considered for any pt grade ll or lll esophageal injury.
5. Diagnostic Endoscopy should be performed within 12-24 hours of alkali ingestion.
6. Corticosteroids have no role in the management of a case and complication. It is rather harmful.
7. Soluble calcium tablet followed by 10% ca gluconate IV can be given in acid ingestion.
8. 1% NaHCO3 irrigation may be given in eye involvement with steroid eye drops.
( Ref. National guideline for management of poisoning)

5. Dhatura Poisoning
Management:
1. NPO TFO
2. Stomach wash with in 1 hour
3. Clearing of the airways
4. O2 inhalation 4-6 L/min
5. Infusion 5% DNS 1000 + 5% DA 1000 cc i/v @ 20 drops/ min.
6. Inj. Omeprazole 40 mg iv slowly stat. & B.D.
7. Physostigmine 0.5 mg to 1 mg s/c stat.
8. Paracetamol suppository
9. Tepid sponging
10. Catheterization done for urinary retention. (antibiotic if catheterization is done).

Tips:
1. If stomach is full, no forceful emesis should be tried.
2. Specific antidote: (l) Physostigmine 0.5 mg to 1 mg s/c to antagonise atropine in a single dose. (ll) Prostigmine is more effective and less toxic than physostigmine in same dose. (lll) Pilocarpine 5 mg s/c, though useful, does not counteract the action of Dhatura on brain, can be repeated 2 hourly at early stage of poisoning.
3. Delirium can be treated with short acting barbiturates.
4. To control marked excitement chlorolhydrate or paraldehyde in moderate dose may be given.
5. Repeated purgation is not recommended.
6. Forced diuresis is not encouraged.
7. Light diet, mainly liquid or semi-liquid should be given if the condition is mild.
8. Other symptomatic treatments.

(Ref. National guideline for management of poisoning)

6. Methanol Poisoning
Management:
1. NPO TFO
2. Stomach wash with in 1 hour
3. Clearing of the airways
4. O2 inhalation 4-6 L/min
5. Infusion 5% DNS 1000 + 5% DA 1000 cc i/v @ 20 drops/ min.
6. Inj. Omeprazole 40 mg iv slowly stat. & B.D.
7. Antidode : Ethanol.
Loading dose: 10% ethanol 7.5 ml/kg IV over 30 to 60 mins
Maintaining dose: 10% ethanol 1.96 ml/kg/hr IV.
If IV not available, then
Orally: 95% ethanol, 0.8 ml/kg followed by 0.1 ml/kg/hr can be given.
Maintaining dose : 0.2 ml/kg/hr. This alcohol should be diluted in water or fruit juice.
Tips:

1. Should be hospitalized and must be treated by an ophthalmologist for his visual problems.
2. Stomach wash although advocated, there is no evidence of affectivity with it.
4. In severe cases pt should be incubated and mechanical respiration should be given.
7. Acidosis should be controlled by infusing sodium bi-carbonate.
8. Sedation can be given cautiously to prevent delirium and restlessness.
9. The antidote for methanol poisoning is ethanol.

(Ref. National guideline for management of poisoning.)

7. Puffer fish poisoning
Management:
1. NPO TFO except medication
2. Stomach wash with in 1 hour with 2% sodibicarb
3. Clearing of the airways
4. O2 inhalation 4-6 L/min
5. Infusion 5% DNS 1000 + 5% DA 1000 cc i/v @ 20 drops/ min.
6. Inj. Omeprazole 40 mg iv slowly stat. & B.D.
7. Tab. Ultracarbon 2+ 2 + 2
8. Atropinization and inj. neostigmine has been used for come round from unconsciousness and restoring neurogenic power both sensory and motor.
Tips:
There is no specific antidote, so only symptomatic treatment:
1. Artificial respiration with oxygen inhalation by mask in mild cases and direct ventilatory support and sedation in severe cases.
2. Purgation and forced diuresis to lessen absorbed poison is not recommended.
3. Steroids for life saving measure although contra-indication persists.
( Ref. National guideline for management of poisoning)

8. Opiate Poisoning
Management:
a. NPO TFO except medication
b. Infusion 5% DNS 1000 cc + 5% DA 1000 cc iv @ 20 d/min
c. Tab Ultracarbon 2 + 2 + 2
d. Inj. Omeprazole 40 mg iv slowly stat. & daily
e. Naloxone can be given to reverse the sign of severe poisoning (coma, respiratory depression or convulsion) within a few minutes but it has a short life and the pt may relapse.

Dose: Administer 0.4–2 mg intravenously, and repeat as needed to awaken the patient. Very large doses (10–20 mg) may be required for patients intoxicated by some opioids (eg, propoxyphene, codeine, fentanyl derivatives).
Caution: The duration of effect of naloxone is only about 2–3 hours; repeated doses may be necessary for patients intoxicated by long-acting drugs such as methadone. Continuous observation for at least 3 hours after the last naloxone dose is mandatory.
9. Paracetamol Poisoning
Management
1. NPO TFO except medication
2. Infusion 5% DNS 1000 cc + 5% DA 1000 cc iv @ 20 d/min
3. Tab Ultracarbon 2 + 2 + 2
4. Inj. Omeprazole 40 mg iv slowly stat. & daily
5. Special antidote: N-Acetylcysteine (NAC), Methionine.
Dose:
 Adult: 150 mg/kg IV in 200 ml of 5% DA over 15 mins, followed by
 50 mg/kg IV in 500 ml dextrose over 4 hours, followed by
 100 mg/kg IV in 1000 ml 5% DA over 16 hours.

With established hepatotoxicity, continue NAC treatment 50 ml/kg in 500 ml of 5% DA over 8 hours.
Repeat until prothrombin time and liver enzyme begin to return to normal.

(Ref. National guideline for management of poisoning.)

10. Savlon poisoning
Diagnostic tools:
1. H/O of ingestion of savlon
2. Burning sensation in throat and upper abdomen.
Management:
1. NPO till further order except medication
2. Irrigate exposed eyes with sterile cold water or saline at least for 20 minutes and continue until the pt. returns to normal.
3. Inj. Omeprazole (40mg) 1 vial i/v slowly stat and daily
4. Inj. Amoxicillin (500mg) 1 vial i/v stat & 8 hourly
5. IV infusion
11. OPC poisoning
Management:
1. External decontamination with water.
2. Remove clothing. Avoid contamination with other personnel.
3. Gastric lavage if pt. resent within 1 hour
4. NPO TFO
5. O2 inhalation 4-6 L/min
6. Tab Ultracarbon 2 + 2 + 2 if present within 1 hour
7. Assisted ventilation as appropriate if respiratory failure
8. Infusion 5% DNS 1000 cc + 5% DA 1000 cc iv @ 20 d/min
9. Inj. Amoxicillin 500 mg iv stat. & 8 hourly
10. Inj. Omeprazole 40 mg iv stat. & daily
11. Atropine 0.6-2 mg repeats after 10-25 min upto atropinasation occurs.
12. Pralidoxime chloride 2 g IV over 4 min, repeated at 4-6 hourly
13. Continued catheterization
14. Monitor vital sign

12 Poisonous snake bite
Polyvalent antisnake venom is effective against the following snake’s venom
1. Cobra
2. Krait
3. Russel’s viper
4. Saw scaled viper
Indication of Polyvalent antisnake venom:
1. Neurotoxic signs
2. Rapid extension of local swelling
3. Acute renal failure
4. Cardiovascular abnormalities
5. Bleeding abnormalities
6. Haemoglobinuria / myoglobinuria

Management:
Assesment
Look for sign of envenometion
1. Polyvalent antisnake venom 10 vial + 100 cc 5% DNS or NS iv @ 60 drops/min
2. If Neurotoxic features- Inj. Atropine 1 amp. iv stat. & 4 hourly, then after 15 min. inj. Neostigmine 4 amp. Subcutaneously 4 hourly.
3. Antibiotic- if risk of infection or Endotrachael intubation done.
4. If features of resp. failure-endotracheal intubation.
5. Follow up 15-30 min. interval by- pulse, BP, Respiratory rate, respiratory movement, adverse effects of antivenom
6. In case of haemostatic abnormalities
• Strict bed rest
• Avoid I/M injection.
• Fresh blood transfusion.
• Avoid NSAID or Aspirin for pain
7.Inj. TT & TIG
8. Iv infusion
Criteria for repeating the initial dose of antivenom:
• If no improvement or deterioration after 1-2 hours
• Persistence or recurrence of blood incoagulability after 6 hours.

Non-poisonous snake bite
Management:
• Symptomatic
• No NSAID ( Analgesic Paracitamol)
• No Sedative & anxiolytics
• Follow up 30 min. interval by- pulse, BP, Resp. rate, resp. movement, features of envenomation.
• After 24 hours if no features of envenomation then discharge the pt.

Respiratory System

1. Allergic rhinitis
Diagnostic tools
1. Frequent sudden attack of sneezing
2. Profuse watery nasal discharge
3. Nasal obstruction.
Management:
Following management either singly or in combination..
1. Antihistamine such as Loratidine
2. Sodium cromoglycate nasal spray
3. Nasal steroid spray e.g. Beclomethason diproprionate, Fluticasone or Budesonide
4. Systemic steroid –in which symptoms are severe.

2. Pneumonia
Diagnostic tools:
1. Fever high grade with cough with sputum (rusty)
2. Chest pain- pleuritic
3. On exam. –feature of consolidation like bronchial breath sound present, vocal resonance increased.
Management:
Uncomplicated CAP (community acquired pneumonia)
1. Antibiotic for 7-10 days
Amoxicilin 500 mg 8 hourly or
Clarithromycin 500 mg 12 hourly
2. Tab. Paracetamol

Severe CAP (2 weeks)
1. Diet- Normal
2. Inj. Ceftriaxone (1gm) 1 vial i/v stat. & B.D
3. Tab. Clarin (500mg) 1+0+1
4. Tab. Paracetamol (500mg) 1+1+1
5. If Chest pain NSAID- Diclofenac sodium
6. Assessment of severity
7. Mechanical ventilation if needed
-Respiratory rate 70 5 5

Category -II management

Pre-treatment wt (kg) Intensive phase Continuation phase
Daily
(First 3 months) Daily
(First 2 months) Daily
(Next 5 months)
Numbers of 4FDC tablets Injection
Streptomycin Numbers of
2 FDC tablets Numbers of
Ehambutol (400 mg) tablets
30-37 2 500 mg 2 2
38-54 3 750 mg 3 3
55-70 4 1 gm* 4 4
>70 5 1 gm* 5 5

4FDC means- 4 fixed drug combination. These 4 drugs are….
1. Rifampicin (R) 150mg
2. Isoniazide (H) 75 mg
3. Ethumbutal (E) 400 mg
4. Pyrazinamide (Z) 275 mg

2 FDC means – 2 fixed drug combination. These 2 drugs are-
1. Rifampicin (R) 150 mg
2. Isoniazid (H) 75 mg.

Q. Why 4 drugs are used in intensive phase?
Ans: To kill rapidly proliferating Mycobacteria.

Q. Why 2 drugs are used in continuation phase?
Ans: To kill the dormant bacteria.

9. Antitubercular drug induced hepatitis
Diagnostic tools
1. H/O of taking Anti TB drugs
2. Yellow coloration of eye & urine
3. Anorexia, nausea & vomiting
4. Investigation- S. Bilirubin- Increased, SGPT-Increased, Alkaline phosphatase- normal, Exclusion of other causes of hepatitis- by HBsAg, AntiHBC, AntiHBE and USG of hapato billiary system & Bil >1.2 mg/dl, SGPT>2 times than normal
Management:
Treatment is symptomatic
1. Stop the offending drugs till hepatitis subside
2. Complete bed rest
3. Diet- normal
4. Tab. Domperidone(10mg) 1+1+1 (1/2 hour before meal, if vomiting)
5. Cap. Omeprazole (20mg) 1+0+1 (1/2 hour before meal)

Tips:
a) Treatment should be restarted when pt. symptomatically well and S. Bilirubin and SGPT become normal.
b) Where there is no scope to do S. Bilirubin and SGPT then Rx. Can be restarted 14 days after the urine or eye become normal.
Ref: Nation guideline of management of tuberculosis.

10. Pneumothorax
Management:
1. Bed rest
2. O2 inhalation
3. Treatment of the underlying cause if any e.g. Pnemonia, COPD etc.
4. Water sealed drainge(percutaneous needle aspiration)- Indication:
i. Immediate decompression prior to definitive therapy in tension pneumothorax
ii. In open or close pneumothorax- Pt. age 15% of hemithorax or significant dysponea.
5. Intercostal tube drainge
i. Tension pneumothorax
ii. Pneumothorax with underlying chronic lung disease e.g. COPD
iii. In open or close pneumothorax -Pt. age > 50 years with >15 % of hemithorax or significant dysponea
iv. When >2.5 L air aspirated or Pneumothorax persists after percuteneous needle aspiration (water seal drainage).
Indication of Surgery in pneumothorax:
1. In all pt. following a second pneumothorax
2. Following first episode of primary pneumothorax
Surgeries are
-Pleurodosis. (Can be achieved by pleural abrasion or parietal pleurectomy at thoracotomy or thoracoscopy).

Advice:
1. Stop smoking
2. Avoid flying 1-2 weeks following full inflation of lung

11. Empyema thorasics
Management
1. Draining of the pus- intercostals tube drainge
2. Antibiotic iv co-amoxiclav or Cefuroxime plus metronidazole
3. Surgical intervention- if IT tube not providing drainge, when the pus is thick or loculated.
4. Surgical decortication of lung – if gross thickening of the visceral pleura is preventing re-expansion of lung.

12. Sarcoidosis
Diagnostic tool
1. Erythema nodosum
2. CXR (P/A)- Bilateral hilar lymphadenopathy
Management:
1. Avoid sun light exposure
2. NSAID for erythema nodosum
3. Steroid-Prednisolone 20-40 mg/day
Indication:
a) Symptoms severe
b) Hypercalcaemia
c) Pulmonary impairement
d) Renal impairement
e) Uveitis

4. Inhaler corticosteroid in asymptomatic parenchymal sarcoid
5. Topical steroid for mild uveitis
6. Severe disease – MTX 10-20 mg / week
-Azathioprine 50-150 mg/day
-Specific TNF alpha inhibitor
7. Cuteneous sarcoid
a) Chloroquine
b) Hydroxychloroquine
c) Low dose thalidomide

13. Pulmonary hypertension
Management:
1. O2 inhalation
2. All pt. should be anticoagulant with warfarin
3. Diuretics
4. Digoxin
5. Specific treatment
d) High dose calcium channel blocker e.g. Amlodipine
e) Prostaglandins such as epoprostenol (prostacyclin) or iloprost therapy
f) PDE inhibitor Sildenafil
g) Oral endothelin antagonist- Bosentan
6. Atrial septostomy
7. Pulmonary thromboendarterectomy
8. Heart- lung transplantation.

14. Acute severe Asthma
Diagnostic tools:
1. Past H/O of asthma
2. Severe breathlessness with cough
3. Patient unable to talk due to breathlessness
4. On exam. Pulse > 110/min, R.rate- > 25/ min, Pt. May be cyanosed, bilateral poly phonic rhonchi present, but chest may be silent.

Management:
1. Diet- normal
2. O2 inhalation 2-5 L/min
3. Propped up position
4. Nebulization with Normal saline 1.5 cc + Salbutamol solution 0.5 cc stat. and 20 min interval for 1 hour then 1-4 hourly.
5. Inj. Hydrocortisone 100 mg 2 vial iv stat. then 4-6 hourly.
6. Inhaler Salbutamol 200 µgm 2 puff stat. & 6 hourly
7. Inhaler Beclomethasone 250 µgm 2 puff 12 hourly (Gargling after use)
8. Tab. Theophylline 400 mg ½ + 0 + ½.

 NB: IV hydrocortisone can be replaced by oral steroid after 24-48 hours.
 Costly regimen- Inhaler Salmetrol & Fludicasone combination. 2 puff 12 hourly. (gargling after use).
 If pt. can buy only one inhaler then give steroid inhaler.
15. Acute exacerbation of COPD
Diagnostic tools:
1. Age > 40 years
2. Smoking H/O
3. Severe breathlessness with cough
4. Previous H/O of hospitalization
5. On exam. Pulse > 100/min, R.rate- > 25/ min, Pt. May be cyanosed, Breath sound vesicular with prolonged expiration,bilateral poly phonic rhonchi & creps present (if infection).

Management:
3. Diet- normal
4. O2 inhalation 1-2 L/min
5. Propped up position
6. Nebulization with Normal saline 1.5 cc + Salbutamol solution 0.5 cc + Ipratropium bromide solution 0.5 cc stat. and 20 min interval for 1 hour then 1-4 hourly.
7. Inj. Hydrocortisone 100 mg 2 vial iv stat. then 4-6 hourly.
8. Inhaler Salbutamol & Ipratropium bromide combination 2 puff stat. & 6 hourly
9. Inhaler Beclomethasone 250 µgm 2 puff 12 hourly (Gargling after use)
10. Tab. Theophylline 400 mg ½ + 0 + ½.
11. Tab. Azithromycin 500 mg 1 + 0 + 0

NB:
 IV hydrocortisone can be replaced by oral steroid after 24-48 hours.
 Costly regimen- Inhaler Salmetrol & Fludicasone combination. 2 puff 12 hourly. (gargling after use).
Antibiotic should be other than the previous one that was used in last 3 month

Renal system

1. Acute glomerulonephritis (Nephritic Syndrome)
Diagnostic tool
1. Swelling of face, leg & eyelid
2. H/O of skin lesion 1-4 weeks before
3. Oliguria, haematuria, fever
4. On exam. –Puffy face, BP-high, leg edema present
-Bed side urine exam. – proteinuria.
– Haematuria
Management
Treatment is supportive, with control of hypertension, edema, and dialysis as needed. Antibiotic treatment for streptococcal infection should be given to all patients and their cohabitants in poststreptococcal AGN.
1. Diet – Normal, protein, salt, fruit, fluid restricted (previous day out put + 400cc)
2. Tab. Cefuroxime axetil (250mg) (in post streptococcal GN then Phenoxymethyl penicillin)
1+o+1
3. Tab. Frusemide (40mg)
1+1+0
4. Tab. Ramipril (1.25mg)
0+0+1 (gradually increasing the dose to titrate BP)
5. Please maintain input out put chart.
 The inflammatory glomerular injury may require corticosteroids and cytotoxic agents.
 Postinfectious Glomerulonephritis- Corticosteroids have not been shown to improve outcome.
(Ref: Harrison’s principle of Internal Medicine)

2. Nephrotic syndrome
Diagnostic tool
1. Generalized edema
2. Massive proteinuria- Frothy urine
3. 24 hours total urinary protein > 3.5 gm
4. Urin volum- normal
5. Usually haematuria absent
Management
1. Diet – Normal, protein, salt, fruit, fluid restricted (previous day out put + 400cc)
2. Tab. Cefuroxime (250mg)
1+o+1
3. Inj. Frusemide(20mg)
1 amp. I/v stat & 1 amp at 8 a.m. & 4 p.m.
5. Tab. Ramipril (1.25mg)
0+0+1 (gradually increasing the dose)
6. Prednisone, 1 mg/kg/d orally
7. Tab. Atrovastatin (10mg) 0 + 0 + 1 after meal (if hypercholesterolemia)
8. Please maintain input output chart.
Tips:
a) Duration of steroid- usually shorter duration (8 weeks) in children but in adult it may take 20- 24 weeks.
b) Patients with frequent relapses and corticosteroid resistance may need cyclophosphamide or chlorambucil to induce subsequent remissions.
(Ref: Harrison’s principle of Internal Medicine +Ref. CMDT 2010)

3. Acute pyelonephritis
Diagnostic tool
1. High fever with chills & rigor
2. Loin pain, dysuria, haematuria, frequency of micturition
3. On exam. – Temperature high
– Renal angle tenderness present.
Management:
1. Diet –normal
2. Antibiotic 1st line (duration10 days)
-Ciprofloxacin (500mg)
-Co-amoxyclav (500/125mg)
3. Tab. Paracetamol if fever
Antibiotic 2nd choice in seriously ill pt. (duration 7-14 days)
• Cefuroxime iv (750mg) 8 hourly
• Gentamycin iv
(Ref: Davidson’s principle & practice of Medicine 21st edition, page 471)
4. Urinary Tract Infection (UTI)
Diagnostic tools:
1. Dysuria, haematuria, frequency of micturition with fever with chills & rigor
2. Urine R/E- pus cell > 5/HPF
3. C/s- growth > 105

Management:
Antibiotic- 3 days in women, 10 days in men
A. First choice
Trimethoprim 200 mg 12 hourly

B. 2nd choice
• Amoxicilin 500 mg 8 hourly or
• Nitrofuratoin 50mg 6 hourly or
• Ciprofloxacin 100mg 12 hourly or
• Co-amoxyclav (250/125mg) 8 hourly
C. In Pregnancy 7 days
• Cephalexin 250mg 6 hourly or
• Amoxicilin 250mg 8 hourly

(Ref: Davidson’s principle & practice of Medicine 21st edition, page 471)

5. Acute renal failure
Diagnostic tools
• H/O of vomiting or diarrhoea or massive blood loss
• Oliguria or anuria
Management:
1. Diet: Protein, salt, fruit restricted
2. Fluid restricted- fluid intake previous day output + 400 cc
3. Infusion Normal saline if pt. dehydrated
4. Antibiotic in case of infection.
5. Cap. Omeprazol (20mg) 1+0 +1
6. Inj. Frusemide (20mg) 2 amp iv stat. and daily (if feature of fluid retension)
7. Maintain input & output chart
Follow up:
• Pulse
• BP
• Hydration status
• Urine out put
• S. creatinine & blood urea
• ECG
Indication of Renal replacement therapy (dialysis or transplantation) in acute renal failure:
1. Hyperkalaemia K+ >6 mmol/L
2. Fluild overload & pulmonary edema
3. Metabolic acidosis
4. Increased plasma urea and creatinine (urea > 180 mg/dl & creatinine >6.8 mmol/L)
5. Uraemic pericarditis/ uraemic encephalopathy
6. Chronic renal failure
Diagnostic tools:
1. H/O of Hypertension or diabetes
2. Pt. complain of anorexia, vomiting, generalized weakness
3. On exam.- Anaemia present
c) Hypertension present
4. S. creatinine- raised.
Management:
1. Diet: Protein, salt & fruit restricted protein 60 gm daily
2. Tab. Calcium carbonate (500mg) 1+0+1
3. Cap. Cholicalciferol (0.25 µgm) 0+1+0
4. Tab. Ferrous sulphate 1+0+1
5. Treatment of the underlying cause like Hypertension, DM etc.
6. If anemia persists after iron therapy then
Inj. Epoietin (25-50IU/kg body wt. once or twice in a week).

Antihypertensive used in CRF
1. First choice- ACEI, ARB, Non-dihydropyridines CCB (Amlodipin)
2. Alpha receptor blocker
3. Betablocker (Atenolol)
N: B: 1-2 week after giving ACEi or ARB if s.creatinine increased 25 % than previous record then stop ACEi or ARB).
Indication of dialysis in CRF (WHO criteria)
1. Uraemic pericarditis
2. Uraemic encephalopathy or neuropathy
3. Pulmonary edema unresponsive to diuretics
4. Severe hypertension if not control by medical management
5. Severe hyperkalaemia not control by medical management
6. Severe bleeding diathesis
7. S. Creatinine > 12 mg/dl or BUN > 100mg/dl
Tips:
Ccr (creatinine clearance) can be estimated from the formula of Cockcroft and Gault:
Ccr = (140- age) × body weight / 72 × S. creatinine (mg/dl)
For women, the creatinine clearance is multiplied by 0.85 because muscle mass is less.
Staging of CKD
Stages of CKD GFR (ml/min/1.73m2)
Stage 1 ≥90 (with evidence of kidney damage)
Stage 2 60-89
Stage 3 30-59
Stage 4 15-29
Stage 5 <15 or dialysis

N: B: kidney damage means pathological abnormalities or marker of damage, including abnormalities in urine tests or imaging studies. Two GFR values 3 months apart are required to assign stage.

CVS diseases
1. Vasovagal syncope
Diagnostic tools
1. Syncope triggered by reduction in venous return due to
a) Prolonged standing
b) Excessive heat
c) Large meal
2. Head up tilt test +Ve.
Pt. is asked to lie on a table that is then tilted to an angel of 60 to 700 for up to 45 min. while ECG & BP are monitored. A positive test is characterized by bradycardia and/ or hypotension associated with typical symptoms.
Management:
I. Life style modifications
i) Salt supplementation
ii) Avoid prolonged standing
iii) Correct dehydration
iv) Avoid missing meal
II. Pt. resistant to life style measure
i) Fludrocortisone
ii) Beta blockers
iii) Disopyramide
3. Dual chamber pace maker if symptoms due to bradycardia.

2. Acute pulmonary oedema
Management:
1. Propped up position
2. O2 high flow 4-6 L/min via face mask
3. Administer Nitrates such as iv GTN 10-200 µg/min or buccal GTN 2-5 mg titrated upwards every 10 min, until clinical improvement occurs or systolic BP falls to 100 mm of Hg.
In other pt. diuretics should be stopped for 24 hours & the ACEi start at low dose.

ACEi Starting dose Target dose
i) Enalapril 2.5 mg 12 hourly 10 mg 12 hrly
ii) Ramipril 1.25 mg daily 10 mg daily.

4. ARB Have similar effect to that of ACEi
Starting dose Target dose
Losarton 25 mg/day 100 mg/day.

5. Combined ACEi & ARB
Indication-HF pt. in those with recurrent hospitalization for HF.
6. Beta blocker therapy
More effective than ACEi in reducing mortality. Bisolol starting dose at 1.25 mg daily increase gradually over 12 weeks to a target maintainance dose of 10 mg daily.
7. Digoxin
To provide rate control
Also in NYHA III, IV
8. Amiodarone
– Effective in pt. of symptomatic arrhythmia
– Should not be used in asymptomatic arrhythmia.
4. Valvular heart disease

Mitral stenosis
Management
Medical management of all valvular diseases is almost same
1. Diet- normal
2. Avoid strenuous exercise
3. O2 inhalation sos
4. Tab. Penoxymethyl penicillin (250mg) 1 + 0 + 1
5. Tab. Frusemide (40mg) 1+0+0
6. Tab. Digoxin 0.25mg 0+0+1 if Atrial fibrillation
7. Tab. Ecospirin (75mg) 0+1+0 (P/C) if Atrial fibrillation
8. In MR ACEI should be given
9. In AR systolic BP should be controlled with Nifedipine or ACEi
Indication of surgery in Mitral stenosis
1. Patient symptomatic despite medical treatment
2. If pulmonary hypertension develops
3. Severe mitral stenosis
4. Pregnancy
2 types of surgery can performed in Mitral stenosis
1. Valvuloplasty
2. Valve replacement
Indication of mitral valvuloplasty in mitral stenosis
1. Significant symptom
2. Isolated MS
3. No (trivial) MR
4. Mobile, non-calcified valve/ subvalve apparatus on Echocardiogram
5. Left atrium free of thrombus
Indication of mitral valve replacement in mitral stenosis
1. MS with MR
2. Rigid & calcified mitral valve cups
Contraindication of surgery
1. Active rheumatic carditis

Mitral regurgitation
Indication of surgery in Mitral Regurgitation (valve replacement or repair)
1. Worsening symptoms
2. Progressive cardiomegally
3. Echocardiographic evidence of deteriorating left ventricular function.

Aortic stenosis
Indication of surgery in Aortic stenosis
1. Development of angina
2. Development of syncope
3. Symptoms of low cardiac output
4. Heart failure
Pt. with moderate to severe stenosis is evaluated every 1-2 year with Doppler Echocardiography to detect progression of severity.

Indication of surgery in aortic regurgitation
1. Symptomatic pt.
2. Asymptomatic pt. should be followed up annually with Echo for evidence of increasing ventricular size, if this occurs or if the end systolic dimension increases to ≥ 55mm the aortic valve replacement should undertaken.

5. Myocardial infarction
Diagnostic tools
1. Classical chest pain > 30 min.
2. ECG changes
3. Biochemical markers e.g. Troponin I.
For diagnosis 2 criteria should be present.
• ECG changes
 ST elevation
 New onset left bundle brunch block
 Evolution of ‘Q’ wave
ECG changes may be isolated or in combination
• Biochemical markers
 CK-MB > 2 fold increase
 Troponin I or T raised level indicate myocardial necrosis.
Management:
1. Complete bed rest
2. Diet- liquid to semisolid
3. O2 inhalation 4-6 L/min
4. GTN spray 2 puff sublingually stat. & sos
5. Tab. GTN SR 2.6 mg 1/2 + 0 + 1/2 + 0
6. Tab. Ecospirin (75mg) 4 tab. Stat. & Tab. Clopidogrel (75mg) 4 tab. Stat.
Then
Tab. Clopidogrel & Aspirin 0 + 1 +0 (after meal)
7. Cap. Omeprazole (20mg) 1 + 0 + 1 ( before meal)
8. Tab. Metoprolol (50 mg) ½ +0 + ½
9. Tab. Ramipril ( 1.25 mg) 0 + 0 +1
10. Tab. Atrovastatin 10 mg 0 + 0 + 1 after meal
11. Inj. Morphine 3 mg iv stat. & SOS (may be repeated after 15 min.)
12. Inj. Stemetil 1 amp. Im stat. Along with Morphine
13. If pt. present with in 12 hours then thrombolysis with Streptokinase or PCI
14. Management of Risk factors e.g. Hypertension, DM etc.
15. Continuous monitoring with pulse rate, rhythm & BP

Mobilization and rehabilitation
 In uncomplicated cases
a) Sit on chair on 2nd day
b) Walk to toilet on 3rd day
c) Return to home on day 5 to 7
d) Gradually increasing activity & return to normal work in 4 to 6 week
 In complicated cases
-Process of mobilization & rehabilitation varies & depends upon the pts functional capacity.

Endocrine system
1. Hypoglycemia
Diagnostic tools
1. H/O of diabetes Mellitus
2. H/O of treatment with Insulin or Secretogogues (e.g. Secrin, Consucon, Limpet etc)
3. H/O of missed or delayed meal
4. Pt. complain headache, dizziness, profuse sweating, palpitation, confusion, drowsy, unconscious
5. On exam.- Bilateral planter extensor
6. Urgent Blood glucose- < 45 mg/dl or 14mmol/L, Keton body on urine present.

Other urgent investigation
I. S. Electrolytes
II. Blood & Urine keton bodies
III. S. creatinine
IV. CBC & Blood culture

Management:
1. NPO TFO
2. O2 inhalation 4-6 L/min
3. Infusion Normal saline
1 L over 30 min.
1 L over 1 hour
1 L over 2 hour
1 L over next 2-4 hours
4. When blood glucose <15.00 mmol/L (270mg/dl) then switch to 5% DA 1 Litre 8 hourly
If pt. still dehydrated then contd. Normal saline and add 5% DA 1 litre 12 hourly
4. Short acting insulin
a) If infusion pump,is available then infuse @ 3-6 units / hour
b) If pump not available 10-20 units IM stat. then 5-10 units hourly. Hourly fall of blood glucose is in the range of 3-4 mmol/L
c) Usual subcutaneous regimen of insulin may be started when the pt. is stable clinically & biochemically & able to take oral food.

5. Potassium replacement
a) None in the first Litre of i.v. fluid unless <3mmol/L
b) If plasma potassium 5.5 mmol/L do not give potassium
6. Broad spectrum antibiotic
7. Continued catheterization
8. Change the posture 2 hourly.

3. HONK (hyperosmolar non-ketotic coma)

Diagnostic tools
1. H/O of DM
2. H/O of irregular treatment or missed dose of Insulin or drugs
3. Stressful condition e.g. infection, trauma, pregnancy
4. On exam. – Severe dehydration, pulse-tachycardia, BP- Hypotension.
5. Investigation- Blood sugar- > 33 mmol/L
a. No keton body in urine
b. Hyperosmolality (> 320 mOsm/ kg)

Hyperosmolality can be calculated by
= 2[Na+] + 2[K+] + [glucose] + urea (all in mmol)
{ Normal osmolality is 280-300 mOsm/kg}

Management:
Same as DK but less insulin is required.
(Ref: Davidson’s principle & practice of Medicine)

4. Cushing syndrome
Management:
Medical treatment before surgery
1. Metyrapone and ketokonazole- the dose should be titrated against 24 hour free urine cortisol level.
2. Treatment of the underlying cause.

Cushing disease
1. Transphenoidal surgery
2. If unsuccessful then bilateral adrenalectomy
Nelson syndrome can be prevented by pituitary irradiation.
5. Addisons disease
Management:
1. Diet- normal
2. Tab. Hydrocortisone 15 mg at morning & 5 mg at 6pm
3. Fludrocortisone 0.05-0.1mg daily

Follow up:
1. Pulse
2. BP
3. S. electrolytes

Advice:
1. If fever double the dose
2. In vomiting inj. Should be given if can not swallow tablet
3. Minor surgery Inj. Hydrocortisone 100 mg im with premedication.
4. Major surgery- Inj. Hydrocortisone 100 mg im 6 hourly until able to take oral tablet
5. Pt. should carry steroid card
6. Bracelet.
6. Addisonian crisis
Management
1. NPO TFO
2. O2 inhalation
3. Infusion normal saline 1000 cc iv @ 30d/min.
4. Infusion 10 % DA 1000cc iv @ 20d/min.
5. Inj. Hydrocortisone 100mg iv stat then im 6 hourly
6. Antibiotic
7. Treatment of the underlying cause.

7. Phaeochromocytoma
Management
a. Definitive treatment is surgery
b. Preparation of pt. before surgery minimum for 6 week
c. Control of HTN by Alpha blocker Phenoxybenzamine 10-20mg orally 6-8 hourly. If tachycardia occurs add betablocker –Propanolol or Labetalol
d. During surgery- Sodium Nitroprusside & short acting alpha antagonist Phentolamine are used to control HTN
e. Postoperative period Hypotension should be managed by -Fluid & Noradrenaline infusion.
8. Hypopituitarism
Management
1. Glucocorticoid replacement
2. Thyroxine 100-150 µgm daily (before this steroid must be given)
3. Sex hormone in men of any age & in female <50 years
4. GH in children & adolescent S/C inj.
5. Treatment of the underlying cause.

9. Prolactinoma
Management:
1. Dopamine agonist (Bromocryptine 1st line drug)
2. Surgery 2nd line treatment.

10. Acromegaly
Management:
1. 1st line treatment is surgery
2. 2nd line treatment is…..
a) Bromocryptine
b) Somatostatin analogue (Octreotide, Lanreotide) slow releasing inj. Every few weeks interval
c) GH receptor antagonist Pegvisomant indicated in whom GH & IGF1 fail to suppress sufficiently by Somatostatin analogue.
11. Diabetes insipidus
Management:
Cranial DI
1. Desmopressin nasal spray 5 µgm in morning & 10 µgm at night. In sick pt. im inj.

Nephrogenic DI
1. Bendroflumethazide 5-10mg/day
2. Amiloride 5-10mg/day
3. Indomethacin 15 mg 8 hourly.

12. Amenorrhoea
Management:
1. Exclude physiological cause e.g. Pg. Menopause etc.
2. Decrease exercise, work load
3. Weight gaining if under weight.

13. Thyrotoxic storm
Management
1. Diet – normal
2. Infusion Normal saline 1000c iv @ 20d/ min
3. Tab. Propanolol 80 mg 6 hourly or 1-5 mg iv 6hourly
4. Sodium ipodate 500mg orally or Dexamethasone 2 mg 6 hourly + Amiodarone
5. Carbimazole if can not take orally then give per rectally
6. Antibiotic
1. Thyrotoxicosis
Management
1. Pt. under 40 years- Tab. Carbimazole 40 -60 mg daily, when pt. euthyroid then 5-20mg for 18 months. If replase occur then –surgery.Subtotal thyroidectomy. Pt. should make euthyroid before surgery by Potassium iodide 60 mg 8 hourly for 2 weeks.
2. If pt. over 40 years – Radio 131I ablation.
Antithyroid drugs
I. Carbimazole 40-60mg daily
II. Methimazole
III. Propylthiouracil (400-600mg daily)

3. Surgery is indicated
Larg goiter.

Note:
 Subjective improvement occur 10-14 days
 Patient biochemically euthyroid at 3-4 weeks. At this time carbimazole should be given at a dose of 5-20mg daily for 12- 15 months.

Thyrotoxicosis in pregnancy
1. Tab. Propylthiouracil 150 mg/day (larger dose cause fetal hypothyroidism).
2. Surgery- if poor compliance. It should be done at 2nd trimester.

15.Graves opthalmopathy
Management
1. Reassurance
2. Methylcellulose eye drop & gell
3. Side shield attached spectacle
4. Prednisolone
5. Sometimes orbital irradiation
6. If loss of visual acquity then urgent surgical decompression.
16. Hypothyroidism
Management
1. Diet – normal
2. Tab. Thyroxine (50µgm) 1 + 0 + 0 ( ½ hour before breakfast)
After 3 weeks
2 + 0 + 0 (½ hour before breakfast)
After 6 week do T3, T4, and TSH then adjust dose of Thyroxine level.
3. Antilipid drugs if hyperlipidaemia.

Note:
1) pt. feel better wuth in 2-3 weeks
2) Reduction in weight & periorbital puffiness occurs quickly
3) Restoration of skin & hair texure and resolution of any effusion take 3-6 months.

Hypothyroidism in IHD
Management
1. Diet- normal, avoid fatty & salty food
2. Tab. Thyroxine (50µgm) 1/2 + 0 + 0 ( ½ hour before breakfast)
Starting dose should be minimum because it can aggravate or precipitate IHD.
Hypothyroidism in Pregnancy
Management
Extra 50µgm/day is required than maintenance dose . Because placenta metabolise thyroxine & increase Thyroxine binding globulin in pregnancy.
T3, T4 & TSH should be assessed in every trimester.
Increased dose of thyroxine is required in the following condition
1. Anticonvulsant drugs
2. Rifampicin
3. Chloroquine
4. Sertraline
5. Aluminium hydroxide
6. Ferrous sulphate
7. Calcium carbonate
8. Malabsorption
9. Pregnancy
17. Myxoedema coma
Diagnostic tools
1. Elderly pt.
2. H/O hypothyroidism
3. Altered consciousness
4. Temperature as low as 25oC.
Management
1. Slow rewarming
2. NG tube feeding
3. O2 inhalation
4. Infusion 5% DNS/ NS
5. Broad spectrum antibiotics
6. Inj. Triiodothyronine (20 µgm) iv stat & 8 hourly, when pt. can take orally then Tab. Thyroxine (50µgm) 1 + 0 + 0 ( ½ hour before breakfast)
7. Inj. Hydrocortisone 100mg im 8 hourly.

Infectious disease
1. Chicken pox in adult or in children
Management
1. Diet – normal
2. Antihistamine
3. Antibiotics
4. Antiviral- oral Aciclovir 800mg 5 times daily for 5 days
In immunocompromised host/ pregnant women Aciclovir 5 mg/kg 8 hourly until pt. improving then complete therapy with oral therapy until all leishon crusting over.
 Visceral involvement (non- CNS) – Aciclovir 5 mg/kg 8 hourly for 7 days.
 Severe complications like encephalitis/ disseminated infection- Aciclovir 10 mg/kg 8 hourly for 14-21 days.
 Lotion claamilon-apply loacaly

2. Shingles or Herpes Zoster
Management
1. Diet – normal
2. Antiviral- oral Aciclovir 800mg 5 times daily
3. Tab. Amitryptylline 25-100mg daily
4. Analgesic –NSAID
Treatment & doses as for chicken pox but typically duration 7-10 days.

3. Infectious Mononeucleosis
Management
1. Diet – normal
2. Antibiotic- penicillin, Avoid Amphicillin or Amoxicillin
3. Steroid – inj. Hydrocortisone 100 mg iv stat. & 6 hourly if pharyngeal edema
4. Return to work governed by pt. physical fitness.

4. Dengue fever
Management
1. Diet – normal, plenty of fluid & home made fruit juice intake
2. Tab. Paracetamol
3. Avoid NSAID, Steroid
4. Fluid management

5. Leptospirosis
Management
1. Diet- normal, salt, fruit. Protein restricted
2. BT if bleeding manifestation
3. Treatment of renal failure
4. Cap. Doxicycline 100 mg 1 + 0 + 1 0r inj. Ceftriacone 1 gm daily
5. If uveitis then oral steroid.
6. Tab. Paracetamol

6.Enteric fever
Management
1. Diet- normal
2. Tab. Paracetamol
3. Antibiotic
Antibiotics that can be used in Enteric fever are—
1. Co-trimoxazole 2 tab. 12 hourly
2. Ciprofloxacin 500 mg 12 hourly
3. Ceftriaxone 2 gm 12 hourly
4. Azithromycin 500 mg daily
Duration of treatment is 14 days.

7. Leprosy
Management
Paucibacillary
1. Diet- normal
2. Tab. Daposone 100mg 1 +0 + 0 ….6 months
3. Tab. Rifampicin 600mg 1 + 0 + 0 one Tab. Monthly for 6 months

Multibacillary
Monthly basis for 12 months
1. Tab. Rifampicin 600mg 1 + 0 + 0
2. Tab. Clofazimine 300mg 1 + 0 + 0
Daily basis for 12 months
1. Tab. Dapsone 100mg 1 tab. daily
2. Tab. Clofazimine 50mg 1tab. daily.
Paucibacillary with single lesion
1. Tab. Ofloxacin 400mg- single dose
2. Tab. Rifampicin 600mg-single dose
3. Tab. Minocycline 100mg- single dose.
8. Rickettsial infection
Management
1. Tetracycline 500mg 6 hourly Or
2. Doxycyclline 100mg 12 hourly Or
3. Chloramohenicol 500mg 6 hourly Or
4. Blood transfusion if haemorrhage
5. Sedation if delirium occurs
Duration of treatment is 7 days.
9. Giardiasis
Management
1. Tinidazole 2 gm stat.
Or
Metronidazole 400mg 8 hourly for 10 days.

10. Filariasis
Management
1. DEC 6 mg /kg daily in 3 divided doses for 12 days.
2. In tropical pulmonary eosinophillia same dose of DEC for 14 days.
Or
3. 300mg DEC single dose
11. Syphilis
Management
Antibiotic- choice Penicillin
Doxicycline if allergic to penicillin except in pregnancy
Azithromycin is a further alternative.

Cure indicated by resolution of clinical sign & decline of non-treponemal test (VDRL) usually to undetectable levels with in 6 months of primary syphilis & 12- 18 months of 2ndary syphilis.
Syphilis in pregnancy
Penicillin is choice.
Erythromycine if allergic to penicilline.
Ceftriaxone 250mg im for 10 days.

12. Gonorrhoea
Management
Uncomplicated
Cefixime 400mg stat. or
Ciprofloxacin 500mg stat. or
Ofloxacin 400mg stat.
Complicated
Quinolone resistance
Ceftriaxone 250 mg im stat or
Spectinomycin 2 gm im stat
In pregnancy & breastfeeding
Cefixime
Ceftriaxone

13. Chlamydial infection
Management
Standard regimen
Azithromycin 1gm single dose or
Doxycycline 100mg B.D. for 7 days.
Alternative regimen
Erythromycin 500mg 6 hourly for 7 days or
Ofloxacin 200 mg 12 hourly for 7 days.

14. Malaria
Uncomplicated
Management:
1. Diet –normal
2. Tab. Artemether & Lumefentrin (Coartem) 4+0+ 4 (for 3 days) (1st line drug)
3. Tab. Paracetamol (500mg) 1+1+1
 Situations where Coartem can not be given…..
a) Pregnancy in first trimester
b) Children 25 kg body wt.) 50 mg morning and evening after meal
• Patients (95%.
Treatment D:
Sodium Antimony Gluconate for PKDL cases
Dose:
20 mg/kg/day in IM route.
Total 6 cycles.
Each cycle consists of 20 days treatment.
Should be an interval of 10 days in between 2 cycles.
Essential to weight the pt every time before starting a new cycle.

Ref: National guideline of diagnosis & management of Kala-azar.

Alimentary tract Disease:

1. Hiccup
Management:

1. Eating 1 TSF of dry granulated sugar.
2. Interruption of the respiratory cycle by breath holding, Valsalva maneuver or rebreathing into a bag.
3. Irritation of the diaphragm by holding knees to chest
4. Tab. Baclofen 1 + 1 + 1
5. Inj. Chlorpromazine 25mg/ml 1 amp. i.m. stat. & B.D. (Before giving LFT & Renal function test should be done)
6. Treatment of the underlying cause.
Other drug can be used treatment
1. Other agents -phenytoin, carbamazepine, benzodiazepines (lorazepam, diazepam), metoclopramide, baclofen, gabapentin, and occasionally general anesthesia.

( Ref. CMDT 2010)

2. Oral ulcer
Management
1. Topical steroid- 0.1% Triamcinolone in orabase (Kenacort oral base )
Or
Choline salicylate 8.7% gel
2. Rarely pt. with very severe recurrent apthous ulcer may need oral steroid.

3. Oral Candiasis
Diagnostic tools
1. Occurs usually in immunocompromised pt. like DM, cytotoxic drugs, steroid, old age etc.
2. White patch in mouth
Management:
1. Nystatin or Amphotericin suspension or Lozens
2. Resistant cases or immunocompromised pt. may require oral fluconazole.

4. Achalasia Cardia
Treatment option:
1. Endoscopic force full pneumatic dilatation
2. Endoscopically directed Botulinum toxin inj. In to the lower oesophageal sphincter
3. If replase occur then surgery- myotomy (Heller’s operation either laparoscopically or open).

5. Gastro Esophagial Reflux Disease( GERD)
Management
1. Omeprazole 20 mg 1 + 0 +1
6. Peptic Ulcer Disease (PUD)
Management
1. Avoid smoking, Aspirin, NSAID
2. H. pylori eradication therapy… duration 7- 14 days.
Cap. Omeprazole 20 mg 1 + 0 +1 ½ hour before meal
Cap. Amoxicillin 500mg 2 + 0 + 2
Tab. Clarithromycin 500mg 1 + 0 + 1
3. Maintainance dose of Omeorazole 20 mg daily.
7. Zolinger- Ellusion syndrome
Diagnostic tools:
1. Severe upper abd. Pain, diarrhea, statorrhoea
2. Poor response to ulcer therapy
3. Endoscopy shows- severe & multiple ulcer in post bulbar duodenum, jejunum & oesophagus.
Management:
1. PPI- larger dose 60- 80mg daily
2. Somatostatin analogue- Inj. Octreotide subcutenously
3. If localized tumor found then resection of the tumor.

8. Non-ulcer dyspepsia (NUD)
Diagnostic tools:
1. Age 6 cm
2. Those whose clinical & Laboratory measurements deteriorate
3. Those not respond after 7-10 days maximal medical treatment.

Maintainance of remission
1. Oral aminosalicylates- Mesalazine or Balsalazine
Sulphalazine has higher side effects but choice in pt. with associated arthopathy. Pt. who frequently relapses despite Aminoslicylate is treated with thiopurines.

13. Irritable bowel syndrome ( IBS)
Diarrhea predominant
Management:
1. Reassuarrance
2. Avoid legumes & excessive dietary fibre
3. Still symptomatic –Loperamide 2-8 mg daily
4. Still symptomatic- Amitryptylline 10 -25 mg at night
5. Still symptomatic-
i) Relaxation therapy
ii) Biofeedback
iii) Hypnotherapy
Constipation predominant
Management:
1. Reassurance
2. High roughage diet
3. Still symptomatic- ispagula, Lactulose
4. Still symptomatic-
i. Relaxation therapy
ii. Biofeedback
iii. Hypnotherapy

Pain & bloating
ManageMent:
1. Mebevarine
2. Peppermint oil
3. Alverine
4. Still symptomatic- Amitryptylline 10- 25 mg at night, Probiotics, Dietary change
5. Still symptomatic-
a. Relaxation therapy
b. Biofeedback
c. Hypnotherapy
14. Anal fissure
Management:
1. Avoid constipation
2. Increase fluid intake
3. Nitric oxide & 0.2% GTN or deltiazem ointment
4. Resistant case- inj. Botulinum toxin
Surgery- Lateral internal anal sphincterotomy or advancement anoplasty.

Haematology
1. Blood transfusion reaction
a) Febrile reaction
Diagnostic tools
 Pt. complain of fever, chills & rigor
 Pt. otherwise normal
Management:
1. Stop the transfusion
2. Paracetamol tab. Or suppository
3. Restart the transfusion at a slower rate
4. Observe the pt. more frequently.

b) Urticaria
Mild allergic reaction
1. Stop the transfusion
2. Give chlorpheniramine 10 mg iv slowly
3. Restart BT at a slower rate
4. Observe frequently.

c) Severe allergic reaction
Diagnosttic tools
1. Bronchospasm, abdominal pain
2. Angioedema, hypotension
Management:
1. Discontinue the transfusion
2. Give Chlorpheniramine 10 mg iv slowly
3. O2 inhalation
4. Nebulize with Salbutamol
5. If severe bronchospasm or hypotension then give inj. Adrenaline 0.5 mg i.m.
6. Send clotted blood sample to the transfusion laboratory
7. Take down blood unit & giving set & return intact to blood bank with all other used/ unused unit.

d)ABO incompatibility
Management:
1. Take down blood unit & giving set & return intact to blood bank with all other used/ unused unit
2. Start i.v. saline infusion
3. Monitor urine out put- maintain urine out >100ml/ hour. Give Frusemide if urine output fall
4. Treat DIC with appropriate blood products
5. Inform hospital transfusion department immediately.
3. Iron deficiency anemia
Management:
1. Diet- iron containing foods like Lal sak, kochu sak etc
2. Tab. Ferrous sulphate 200mg 8 hourly for 3-6 months. If pt. intolerant to ferrous sulphate then Ferrous sulphate 12 hourly or Ferrous gluconate 300 mg 12 hourly
3. Blood transfusion-indication
i) If pt. have angina
ii) Heart failure
iii) Evidence of cerebral anoxia
4. Parentral iron-indication
i) Malabsorption
ii) Chronic gut disease

Follow up:
1. Hb%- Hb% should be rise 1 gm/dl/week
2. Reticulocyte count- Reticulocytosis is evident after 7-10 days.
4.Megaloblastic anaemia
Management:
1. Diet- normal
2. Inj. Hydroxycobalamine 1000 µg i.m. five doses 2-3 days apart then 3 monthly life long
3. Tab. Folic acid 5 mg 1 tab daily for 3 week, then 1 tab. Weekly for life long
4. Ferrous sulphate 200 mg 8 hourly, if initial responses is not maintained & PBF is dimorphic.

5.Spleenectomized Pt.
Management:
1. Vaccinate the pt.
 Pnemococcal
 H.inluenza type B
 Meningococcus C
 Influenza
Vaccination should be done 2-3 weeks before elective surgery. If emergency surgery is done then vaccination should be done after surgery.
2. Pneumococcal reimmunization should be done every 5 yearly
3. Influenza reimmunization should be done yearly basis.
4. Penicillin V 500 mg 12 hourly life long
5. Should carry Bracelet or card.

6.Autoimmune Haemolytic anaemia
Management:
1. Steroid –prednisolone 1 mg/kg/day orally, when Hb% normalized, reticulocytosis resolved dose of steroid should be reduced over 10 weeks
2. Blood transfusion- when developed heart failure or unabated fails in Hb%
3. Splenectomy- if haemolysis fails to respond to steroid or can only be stablished by larger doses.
4. Azathioprine or cyclophosphamide-if splenectomy is not appropriate.

7.Paroxyamal nocturnal haemoglobinuria (PNH)
Diagnostic tools:
 Pt. complain –red brown color urine particularly in morning
 Urine R/E- haemoglobinuria

Management:
1. Diet- normal
2. Blood transfusion
3. Treatment of thrombosis
4. Recently anticomplement C5 monoclonal Ab Ecluzimab is used.

8. Sickle cell anemia
Management:
1. Tab. Folic acid 5 mg 1+ 0 + 0
2. Tab. Penicillin V
3. Hydroxycarbamide
4. Vaccinate against Pneumococcus, H. influenza & Hepatitis B.
Treatment of vaso-occlusive crisis
1. O2 inhalation
2. Rehydration with Normal saline
3. Antibiotic
4. Analgesia with opiate
5. Exchange transfusion
 in life threatening crisis
 Or to prepare the pt. for surgery.

9. Chronic myeloid leukaemia
Chronic phase
1. First line therapy- Imatinib,
If fail to response or progress on therapy- Dasatinib or Nalatinib, Bone marrow transplantation (allogenic)
Or
Hydroxyurea or Hydroxycarbamide or Interferon.
2. Hydroxyurea- if pt. can not afford Imatinib.
Accelerated or blast crisis phase
1. Imatinib
2. Hydroxycarbamide & low dose cytarabine. If fail to response or progress on therapy- Dasatinib or Nalatinib, Bone marrow transplantation (allogenic).

10. Chronic Lymphatic leukaemia
Stage A
No treatment is required.
Stage B & C
1. Chlorambucil, recently Fludarabine plus Cyclophasphamide
2. Corticosteroid- in bone marrow failure or autoimmune cytopenias
3. Blood transfusion if anaemia or thrombocytopenia
4. Antibiotic – infection
5. Radiotherapy-if lymph node causing discomfort or local obstruction & symptomatic splenomegally
6. Splenectomy- to decrease autoimmune destruction of RBC, Hypersplenism & to relieve massive splenomegally.

11. Myelodysplastic syndrome
Management:
1. Blood transfusion
2. Platelet transfusion
3. Erythropoietin & GCSF
4. Allogenic bone marrow transplantation in younger pt.

12. Multiple myeloma
Management:
Asymptomatic –no treatment is required
Symptomatic
1. Plenty of fluid intake
2. NSAID to relieve pain
3. Bisphosphonates
4. Allopurinol
5. Plasmapharesis-in hyperviscosity
6. Chemotherapy
1st line –Thalidomide
Older pt. – Thalidomide plus Melphalan & Prednisolone
In younger pt. -Thalidomide plus allogenic BMT.
7. Radiotherapy- localized bone pain not responding to simple analgesic & pathological fracture, spinal cord compression.

13. Aplastic anaemia
Management:
1. Diet- normal
2. Antibiotic
3. Immune suppressive therapy for older pt. with-Ciclosporin & Antithymocytic globulin
4. Younger pt. < 30 years – allogenic BMT.
14. Myelofibrosis
Management:
1. Diet- normal
2. Tab. Folic acid
3. Blood transfusion
4. Hydroxycarbamide
5. Splenectomy- if symptomatic pancytopenia, enlarged spleen, hypersplenism
6. Allogenic BMT in younger pt.
15. Polycythaemia Rubra vera
Management:
1. Diet- normal
2. Venesection 400-500 ml every 5-7 days until PCV 30 thousand do not require treatment
2. First line therapy for pt. with spontaneous bleeding
A. Prednisolone 1 mg/ kg daily
B. If response to steroid is slow & severe haemostatic failure
 Prednisolone & IVIg
Or
Intravenous anti D
C. Persistent or potentially life threatening bleeding should be treated with platelet transfusion in addition to other therapies
D. Splenectomy- if 2 relapses or primary refractory disease
E. If significant bleeding persists despite splenectomy- low dose steroid, immunosuppressive therapy with Rituximab, ciclosporin & Tacrolimus.
17. Haemophilia
Haemophillia A
1. Resting of the bleeding site by bed rest or splint
2. In severe hemophilia A intravenous infusion of factor VIII concentration
3. In mild to moderate hemophilia A Vasopressin receptor agonist DDAVP 0.3 µg/ kg iv or subcutaneously. Alternatively same effect can be achieved by intranasal administration of 300 µg.
4. Prophylaxis – Factor VIII can be administered 2 or 3 times per week.
Haemophillia B
Factor IX concentration intravenous infusion.
18. Acute leukaemia
Diagnostic tool
1. Fever high grade
2. Generalized weakness
3. Bleeding manifestations e.g.- gum bleeding, epistaxis, etc.
4. On exam. –Anaemia, Lymphadenopathy, Bony tenderness, Hepato-splenomegally.

Urgent Investigation:
1. CBC with PBF

Management:( Supportive)
1. Diet- normal
2. Blood transfusion (before BT PBF should be done)
3. Inj. Eracef (1gm) ivial i/v daily
4. Tab. Paracetamol (500mg) 1+1+1
5. If menorrhagia Tab. Premulate N 2+2+2

For specific management referred to Haematologist.

19. Haemolytic anaemia
Diagnostic tool
1. Generalized weakness
2. No fever, bleeding manifestation
3. On exam.
 No lymphadenopathy, No bony tenderness
 Hepatosplenomegally.

Management:
1. Diet – normal
2. BT
3. Tab. Folison 1+0+0

Dietary advice:
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An approach to diagnosis of Anaemia from examination findings:
 Anaemia + Bleeding manifestation + No lymphadenopathy + No bony tenderness + No Hepatosplenomegally ¬– Aplastic anaemia.
 Anaemia + No Bleeding manifestation + No lymphadenopathy + No bony tenderness + Hepatosplenomegally ¬– Haemolytic anaemia.
 Anaemia + Bleeding manifestation + lymphadenopathy + bony tenderness + Hepatosplenomegally ¬– Acute leaukaemia.

MUSCULO-SKELETAL DISEASES
1. Low back pain (LBP)
Management:
1. Reassurance, explanation
2. Analgesic- paracetamol, NSAID, Muscle relaxants
3. Discourage bed rest
4. Low dose TCA e.g. Amitryptylline
5. Refered for Physiotherapy or manipulation- if return to normal physical activity has not been achieved by 6 weeks.
2. Osteoarthritis
Management:
1. Full explanation of the condition
 Established structured changes are permanent
 Pain & function can be improved
2. Exercise- strengthening & aerobic exercise
3. Hot or cold compression
4. Reduction of adverse mechanical factors
– Weight loss if obese
– Shock absorbing foot wear
– Use of walking stick for painful knee or hip OA.
5. Drug
– Paracetamol
– Topical NSAID
– Oral NSAID
6. Intraarticular inj. Of corticosteroid to relieve pain of knee & thumb base OA
7. Surgery
Indication:
i) OA whose pain, stiffness & reduced function impact significantly on their quality of life
ii) Refractory OA (refractory to non-surgical & adjunctive treatment).
Surgeries are- Osteotomy & joint replacement for knee & hip joint OA.
3. Rheumatoid arthritis
Diagnostic tools:
1. Polyarthritis -3 or more joints pain
2. Hand joint involvement
3. Symmetrical arthritis
4. Rheumatoid nodule
5. Morning stiffness > 1 hour
6. Rheumatoid factor (RA test Positive)
7. Radiological changes
8. Symptoms for more than 6 weeks.

4 or more criteria suggest diagnosis of RA.

Management: (ward or practical mx.)
1. Diet : Normal
2. Cap. Indomethacin (25mg) 1+1+1 (after meal)
3. Cap. Omeprazole (20mg) 1+0+1 ( before meal)
4. Tab. MTX (2.5mg) 3+0+0 ( every saturday)
5. Tab. Folic acid 1+0+0 (every sunday)

Rheumatoid arthritis
Management:(Ideal)
1. Rest
2. Passive exercise
3. NSAID
4. DMARD
5. Anti TNF therapy-if disease activity persists despite adequate trial of 2 DMARD including Methotrexate
6. Corticosteroid-Prednisolone 7.5-10 mg daily. To cover delayed onset of action of DMARD
7. Surgery-indication-when medical treatment fail to pain relief or to prevent tendon rupture.
8. Surgeries are
Synovectomy (wrist or finger tendon sheath)
Osteotomy
Arthodosis or arthoplasty
Follow up in pt. getting MTX initially monthly, then every 3 month
1. Clinical improvement
2. Full blood count and LFTs
4. Ankylosing spondylosis
Management:
Non-pharmacological:
1. Explanation & education
2. Daily back extension exercise including a morning ‘warm up’ routine
3. Avoid prolonged period of inactivity work like driving, computer work etc.
4. Swimming is the best exercise.
Pharmacological treatment:
1. NSAID
2. MTX or sulphasalazine if peripheral arthritis
3. Anti TNF therapy for disease inadequately controlled with above measure
4. Oral corticosteroid- in acute uveitis
Surgery
In severe hip, knee, shoulder joint restriction.
5. Reactive arthritis
Management:
1. Rest
2. NSAID
3. Tetracycline
4. Intraarticular inj. for marked synovitis
5. DMARD
 Persistent marked symptom
 Recurrent arthritis
 Severe keratoderma blenorrhagica
6. Ant. Uveitis- topical, oral, subconjunctival steroid.
6. Psoriatic arthritis
Management:
1. Avoid splint & prolonged rest
2. NSAID
3. Intrarticular inj. of steroid to control synovitis
4. DMARD- Methotrexete
5. Anti TNF therapy in whom DMARD fail
6. Retinoid acitretin
7. Photochemotherapy & methylpsoralin and long wave UV light.

7. Gout
Management:
Acute attack
1. Application of ice pack
2. NSAID
3. Oral Colchicine 0.5 mg 6/8/12 hourly
4. Joint aspiration & intraarticular inj. Of steroid
5. For severe oligo-polyarticular attack- parentral corticosteroid.
Long term management:
1. Correction of predisposing factors
2. Weight loss & reduction of excess alcohol intake especially bear
3. Diuretics should be stopped if possible
4. Avoid sea food, read meat
5. Allopurinol initial dose 100 mg daily (50 mg in elderly), gradually increase the dose up to 900 mg daily.
Follow up:
S. uric acid should be measured 3-4 weeks interval.
Advice to the pt:
During initiation of urate lowering drug acute attack may occur but drug should not be stopped.
Tips:
Acute attack during initiation of urate lowering therapy; oral cholchicine or NSAID can be added.

8. Septic arthritis
Urgent investigation:
1. Synovial fluid for Gram staining & culture
2. Blood for FBC & culture
3. Consider sputum, urine culture
Management:
1. Intavenous Flucloxacillin 2 gm 6 hourly for 2-3 weeks then oral for 6 weeks. Change according to C/S
2. If Penicillin allergy then-Clindamycin 450-600 mg 6 hourly
3. If high risk for Gram negative infection then add Cephalosporin
4. Serial needle aspiration 1-3 times per day
5. Pain relieved by- local ice pack, oral or iv analgesic
6. Physiotherapy from the first day
-Regular passive movement progressing to active movement.
9. SLE
General management:
1. Educate the pt.
2. Avoid sun & UV light exposure, employ sun block
3. Avoid smoking
4. Control hypertension & dyslipidaemia
Mild disease (restricted to skin & joints)
1. NSAID
2. If necessary Hydroxy chloroquine 200-400 mg daily
3. Short course of steroid for rash, synovitis, pleurisy & pericarditis.
Life threatening disease
Affecting kidneys, CNS or CVS requires high dose steroid plus immune suppression.
1. A commonly used regimen- Pulse Methyl prednisolone 500 mg -1 gm iv coupled with cyclophosphamide 2 mg/kg iv repeated at 2-3 weekly interval on 6-8 occasion.
Alternatively in renal involvement Cyclophosphamide can be replaced with Mycophenolate mofetil(MMF) with fewer side effects.
2. Folowing control- prednisolone 40-60 mg daily & Azathioprime, MTX or MMF
3. Co-trimoxazole 960 mg thrice weekly to prevent P. carinii infection due to cyclophosphamide
4. Mesna is given with bolous Cyclophosphamide to reduce risk of haemorrhagic cystitis
5. Lupus nephritis with Antiphospholipid syndrome who have had previous thrombosis require life long warfarin.

10. Systemic sclerosis
A) Raynaud’s syndrome with digital ulcer
1. Avoid cold exposure
2. Use of mittens (heated mittens are available)
3. Calcium antagonist or ARB
4. Antibiotic
a. Intermitten infusion of epoprostenol may benefit severe digital ischaemia
B) Ooesophageal reflux
 PPI
 Metochlopramide or domperidon
 Antibiotic for bacterial overgrowth
C) Hypertension-ACEi even also in renal impairement
D) Joint involvement-Analgesic
E) Pulmonary hypertension- Endothelin-1 antagonist ‘ Bosentan’
F) Corticosteroid & cytotoxic drug are indicated in pt. with
– co-existing myositis or
– fibrosing alveolitis.

11. Polymyositis & Dermatomyositis
Management:
1. Oral corticosteroid 40-60 mg daily
2. iv Methylprednisolone 1 gm daily for 3 days in pt. with respiratory or pharyngeal weakness. If thre is a good response steroid should be reduced by approximately 25% per month to maintain dose of 5-7.5 mg
3. Most pt. require additional treatment with Azathioprine & MTX
4. iv immuneglobulin may be effective in refractoryces.

12. Bechet’s Syndrome
Diagnostic tools
1. Oral ulcer deep & multiple
2. Genital ulcer
3. Skin leishon-erythema nodusum or acneform leishon
4. Migratory thrombophlebitis
5. Anterior or posterior uveitis
6. Neurological sign-brain stem involvement, pyramidal tract signs etc.
Management:
1. Oral ulcer- topical steroid preparation
2. Colchicine for erythema nodusum & arthalgia
3. Thalidomide 100-300 mg daily for 28 days & effective for resistant oral & genital ulcer
4. Corticosteroid & immunosuppressive for systemic disease.

13. Polymyalgia Rheumatica (PMR)
Management:
1. Prednisolone 20-30 mg daily gradually reduce the dose 10-15 mg by about 8 weeks ultimately 5-7.5 mg for 12-14 weeks
2. Immunosuppressive like MTX, Azathioprine when steroid require > 7.5 mg/day.

14. Giant cell arteritis
Management:
1. Prednisolone 60 mg daily

15. Osteoporesis
Non-pharmacological treatment
1. Cessation of smoking
2. Moderation of alcohol intake
3. Dietary calcium intake
4. Exercise
Drug treatment
Indication
1. BMD T score below -2.5 or below -1.5 in corticosteroid induced osteoporeis
2.Vertebral fracture irrespective of BMD (except traumatic vertebral fracture)
Drugs used
1. Alendronate 70 mg/ week or Risedronate 35 mg/ week. Orally on empty stomach & no food should be taken up to 30-45 min. of administration
2. Calcium & vit-D
3. PTH- Teriparatide. Superior to Alendronate. It is expensive, rserve for
a) Szevere osteoporesis BMD T score -3.5 to – 4.0 or below
b) Failure to respond adequately to other treatment.
Duration 24 months, after that Bisphosphonate should be used to maintain BMD. Teriparatide should not be used simultinously with Bisphosphonate.
4. Calcitonin- has analgesic properties. Sometimes used short to medium time in pt. with acute vertebral fracture. Dose s/c or im 100-200 U daily or intranasal spray 200 micro units daily.
5. HRT-primarily indicated for prevention of osteoporesis in women with an early menopause & for treatment of women with osteoporesis in their early fifties who have troublesome menopausal symptoms
6. Calcitrol-recently licensed for treatment of osteoporesis
Surgery
 Hip replacement- total or partial, indicated for intracapsular fracture of femoral neck.
 Kyphoplasty-indicated for acute vertebral compression fracture where there is a significant degree collapse & severe pain.
 Vertebroplasty- indicated for painful vertebral fracture which fails to settle by medical treatment.
Follow up:
1. BMD repeat after 2-3 years
2. NTX (N-Telopeptide) respond quickly than BMD.

16. Osteomalasia & Rickets
Management:
1. Respond quickly to treatment with ergocalciferol 250-100 µgm daily.
After 3-4 months treatment can generally be stopped or the dose of vit-D reduce to maintainance level of 10-20 µgm Cholecalciferol daily except in pt. with Malabsorption in whom higher dose may required.
Follow up:
1. Clinical improvement
2. Elevation in 25(OH)D
3. Reduce in PTH.

Neurology
1. Tension type Headache
Management:
1. Explanation of symptoms
2. Avoid precipitation
3. Analgesics-NSAID
4. Muscle relaxation
5. Amitryptyline
6. Phycotherapy.

2. Migrain
Acute attack
1. Identification & avoidance of precipitating or exacerbating factors such as OCP, smoking
2. Analgesic-NSAID or Paracetamol
3. Metochlopramide or domperidon
4. Severe attack- Sumatryptan, 5-HT agonists
5. Frequent attack are prevented with
 Propanolol
 TCA
 Sodium valproate 300-600mg/day or Topiramate 50 -100 mg/day.
3. Status epilepticus
Management:
Clearing the airway
O2 inhalation

Inj. Diazepam 10mg (Sedil) iv or rectally
Can be repeated after 15 min.

If seizure continued after 30min. then
i.v. Fosphenytoin 15mg/kg at 100mg/min.
Or
i.v. Phenobarbital 10mg/kg at 100mg/min.

If seizure still continued after 30min. then
Start treatment for refractory status with intubation with general anaesthesia with Propofol or Thiopental.

Once status controlled start longer term anticonvulsant medication with one of the following-
a) Sodium valproate 10mg/kg i.v. over 3-5 min. Then 800-2000mg/day.
b) Carbamazepine 400mg by NG tube then 400-1200mg/day.

Guideline for choice of Antiepileptic drugs
Epilepsy type 1st line 2nd line 3rd line
1. Partial or 2ndary GTCS Carbamazepine Sodium valproate Phenobarbital
(200-2000mg/day) Phenytoin
2-3 dose/day

2. Primary GTCS Sodium valproate Lamotrigine Phenobarbital
400-2500/day 60-180mg/day 1-2 dose/day
1-2 dose/day Phenytoin
Carbamazepine
4. Acute stroke
Diagnostic tools
• Sudden onset of weakness of one side of the body or loss of consciousness
• No H/O of fever
• On exam. Hemiplegia and planter extensor in that side.
Management:
1. NG tube feeding
2. O2 inhalation 2-4 l/min
3. Infusion Normal saline 1000cc iv @ 10 drops/min
4. Syrp. Amoxicillin 2 TSF TDS
5. Omeprazole sachet 1 sachet dissolve in ½ glass water then take via NG tube 12 hourly
6. Paracetamol suppository (500mg) 1 stick P/R stat. and SOS
7. Cold tepid sponging
8. Continued catheterization
9. Change the posture 2 hourly
10. Care of the mouth, eye, bowel
11. Treatment of underlying cause like DM, Dyslipidaemia etc.

• If pt. is known hypertensive and taking drug regularly then contd. the drug.
• If pt. is not known hypertensive & BP is high then not give antihypertensive. Antihypertensive should be given in the following condition
-In Ischaemic stroke if BP >220/120 mm of Hg
-In Haemorrhagic stroke > 180/ 110 mm of Hg
• If pt. is Diabetic then start insulin
• If pt. is not known diabetic but blood sugar is >11.1 mmol/L then start insulin.

5. Tetanus
Management
1. O2 inhalation stat 4-6 L/min
2. Nurse in a quite room
3. Avoid unnecessary stimuli
4. NG tube feeding 200 ml 2 hourly
5. Infusion 5% DNS 1000 cc i.v. daily
6. Inj. Benzylpenicillin 600mg iv 6 hourly Or inj. Metronidazole if allergic to Penicillin
7. Inj. TIG 12 amp. i.m. stat.
8. Inj. Diazepam (10mg) 1 amp. i.v. stat & B.D.
9. Change the posture 2 hourly

6. Meningo-encephalitis
Diagnostic tools
1. Fever, Headache
2. Alteration of consciousness
3. On exam.- Neck rigidity present
1. Kernig’s sign present
Management:
1. NG tube feeding 200 ml 2 hourly in sitting posture & maintain the posture for 10 min.
2. Inj. Ceftriaxone (2gm) 1 vial i.v. stat & BD
3. Inj. Dexamethasone 2 amp. i.v. 20 min before giving antibiotics stat & 6 hourly for 3 days
4. Omeprazole sachet 1 packet dissolve in ½ glass water through NG tube BD
5. Continued catheterization
6. Change the posture 2 hourly
7. Care of mouth, eye & bowel
8. If short H/O of fever then add Tab. Acyclovir (400mg) 2+2+2+2+2

Pyogenic Meningitis Choice of antibiotic
1. Pt. present with typical meningococcal rash- Inj. Benzylpenicillin 2.4gm iv 6 hourly
2. Adult aged 18-50 years without typical meningoccal rash – Cefotaxime 2 gm iv 6 hourly or Ceftriaxone 2 gm iv 12 hourly.
3. Pt. in whom penicillin resistant pneumococcal infection is suspected- as for (2) but add Vancomycin 1 gm iv 12 hourly or Rifampicin 600mg iv 12 hourly
4. Adult aged over 50 years and those in whom Listeria monocytogen infection is suspected (Brainstem sign, immunosuppression, diabetic, alcoholic)- as for (2) but add Ampicillin 2 gm iv 4 hourly or Co trimoxazole 50mg /kg iv in 2 divided dose.

7. Encephalitis
Diagnostic tools
4. Fever, Headache
5. Alteration of consciousness
6. On exam. – No Neck rigidity
-No Kernig’s sign.
Management:
1. Same as Mningo-encephalitis
2. If convulsion occurs then add Tab. Carbamazepine (200mg) 1+1+1.

8. Trigeminal neuralgia
Management:
a. Carbamazepine up to 1200 mg daily should be started at low dose. Who can not tolerate it add Gabapentin or Pregabaline.
b. Inj. of Alcohol or Phenol in to a peripheral branch of the nerve.
9. Restless leg syndrome
Management:
1. Clonazepam (0.5-2mg) at night
2. Levodopa 100-200 mg or dopamine agonist at night.

10. Subarachonoid Haemorrhage
Management:
1. Nimodipine 30-60 mg iv for 5-14 days followed by 360 mg for further 7 days.
2. Definitive treatment
a. Insertion of platinum coil in to an aneurysm via endovascular procedure
Or
b. Surgical clipping of the aneurysm neck.
AV malformation –surgical removal, ligation, injection of material to occlude the fistula or draining veins.

11. Transverse Myelitis
Management:
1. Diet – normal
2. Inj. Methylprednisolone 1 gm daily for 3 days
3. Omeprazole
4. Continued catheterization

12. Dementia/ Alzheimer;s disease
Management:
1. Donepezil 10 mg daily
2. Antidepressant in depressive pt.

13. Wernick- Korsakoff disease
Diagnostic tools
1. H/O alcoholism, malabsorption, malnutrition, Hyperemesis gravidarum
2. Acute confusional state (W.encephalopathy)
3. Brain stem sign e.g. ataxia, nystigmus & extraocular muscle weakness particularly lateral rectus.
Management:
1. Intravenous Thiamine 2 vial 8 hourly for 48 hours, then oral Thiamine 100 mg 8 hourly
2. Treatment of the underlying cause.

14. Parkinsonism
Management:
1. Levodopa –carvidopa, 50 mg 8 or 12 hourly increased up to 1000 mg/day. This drug improve bradykinesia & rigidity
2. Anticholinergic-improve tremor & rigidity
3. Trihexyphenidyl (benzhexol 1-4 mg 8 hourly)
4. Orphenadrine 50 -100 mg 8 hourly
3. Dopamine receptor agonist
5. Bromocryptine 1 mg initially then 2.5 mg 8 hourly up to 30 mg/day
6. Pergolide 50 µgm (starting dose) increased to 250 µgm 8 hourly up to 3000 µgm/day.
4. Amantadine
-Use in early of the disease when more potent treatment is not required
-To control dyskinesia produced by dopaminergic treatment.
Dose 100 mg 8 or 12 hourly.
5. COMT inhibitors
Entacapone 200 mg with each dose of levodopa. This prolonged the effect of levodopa & allows levodopa dose to be reduced & given less frequently.
6. Surgery
Stereotactic thalamotomy to treat tremor. Now a days need relatively infrequently
7. Physiotherapy & speech therapy.

15. Huntington’s disease
Symptomatic management
7. Tetrabenazine or dopamine antagonists such as sulpride
8. Antidepressants for depressive pt.
9. Psycological support
10. Genetic counselling for the relatives
16. Rabies
Management:
Established disease
1. ICU support
2. Sedation with Diazepam 10 mg 4-6 hourly
3. Chlorpromazine 50-100 mg if necessary
4. Nutrition & fluid by iv or gastrostomy.
Prevention
Pre-exposure prophylaxis – protection is afforded by 2 intradermal injection of 0.1 ml human diploid cell vaccine or 2 intramuscular inj. Of 1 ml, given 4 weeks apart, followed by yearly booster.
Post exposer vaccination before development of sign symptom. For maximum protection hyperimmune serum and vaccine are required.
Safest antirabies antiserum is human rabies immune globulin, the dose is 20 U/kg, half should be infiltrated around the bite and half im at adifferent site from vaccine.
Safest vaccine is human diploid cell vaccine 1 ml is given intramuscularly on days 0, 3, 7,14, 30 and 90.

17. Cerebral abscess
Treatment:
1. Diet – normal
2. Antibiotic
3. Anticonvulsant- Carbamazepine SR 200 mg B.D.
4. Paracetamol if fever
5. Surgery
Burr-hole aspiration or excision-where presence of a capsule may lead to a persistent focus of infection.

Antibiotic choice is guided by following condition
Frontal lobe
Cefuroxime 1.5 gm iv 8 hourly
Plus
Metronidazole 500 mg 8 hourly.
Temporal lobe & Cerebellum
-Ampicillin 2-3 gm iv 8 hourly
Plus
-Metronidazole 500 mg 8 hourly
Plus
Either Ceftazidime 2 gm iv 8 hourly or Gentamycin 5 mg/ kg iv daily.
Any site
H/O penetrating injury
-Flucloxacillin 2-3 gm iv 6 hourly
Or
– Cefuroxime 1.5 gm iv 8 hourly
Multiple abscesses
-Benzylpenicillin 1.8 – 2.8 gm iv 6 hourly if endocardits or cyanotic heart disease.
– Otherwise Cefuroxime 1.5 gm 8 hourly
Plus
Meteronidazole 500 mg 8 hourly.

18. Idiopathic intracranial hypertension
Management:
1. Weigh reducing diet
2. Avoid any precipitating condition or medication
3. Carbonic anhydrase inhibitor-Acetazolamide
4. Repeated LP
5. Optic nerve fenestration or lumbo-peritoneal shunt if
-Pt. failing to respond
-Chronic papilloedema threatens vision.

19. Lumber disc herniation
Management:
1. Back strengthening exercise
2. Early mobilization
3. Analgesic
4. Inj. Of local anaesthetic agent or corticosteroid, if symptoms due to ligamentus injury or joint dysfunction
5. Surgery
-No response to conservative treatment
-progressive neurological deficits develops
-Central disc herniation with bilateral symptoms & signs & distrubnance of sphincter function require urgent surgical decompression.

20. Fascial nerve palsy
Management:
1. Artificial tear & ointment
2. Eye should be tapped shut overnight
3. Prednisolone 40-60 mg daily for 7 days (should be started with in 72 hours).

21. Guillain-Barre Syndrome
Management:
1. Regular monitoring of the pt. with respiratory function, VC & ABG
2. Artificial ventilation if VC 15 mg/dl
c) Prolonged prothrombin time
d) Co-morbidities- like DM, IHD
Criteria of hospital discharge-
a) Substantial symptomatic improvement
b) A significant downward trend in the serum aminotransferase and bilirubin values and
c) A return to normal of the PT
d) Mild aminotransferase elevations should not be considered contraindications to the gradual resumption of normal activity.
( Ref: Harrison’s principle of Internal Medicine + CMDT 2010)

3. Acute liver failure
Hyperacute liver failure- if jaundice to encephalopathy time 2gm/dl in 24 hours).
5. Close monitoring of the pt. with Pulse, BP, and urine out put and Hb%.
6. If bleeding continues then Therapeutic Endoscopy.
Tips
 A systolic blood pressure less than 100 mm Hg identifies a high-risk patient with severe acute bleeding.
 A heart rate over 100 beats/min with a systolic blood pressure over 100 mm Hg signifies moderate acute blood loss.
 A normal systolic blood pressure and heart rate suggest relatively minor hemorrhage.
 In actively bleeding patients, platelets are transfused if the platelet count is under 50,000/mm3 and considered if there is impaired platelet function due to aspirin or clopidogrel use (regardless of the platelet count).
 Uremic patients (who also have dysfunctional platelets) with active bleeding are given three doses of desmopressin (DDAVP), 0.3 mcg/kg intravenously, at 12-hour intervals.
 Fresh frozen plasma is administered for actively bleeding patients with a coagulopathy and an INR > 1.5.
 In the face of massive bleeding, 1 unit of fresh frozen plasma should be given for each 5 units of packed red blood cells transfused.
 Predictor of rebleeding- clinical predictors of increased risk of rebleeding and death include
a. Age > 60 years,
b. Co morbid illnesses,
c. Systolic blood pressure 100 beats/min, and
e. Bright red blood in the nasogastric aspirate or on rectal examination.
Features of active bleeding: Patients with active bleeding manifested by hematemesis or bright red blood on nasogastric aspirate, shock, persistent hemodynamic derangement despite fluid resuscitation, serious co-morbid medical illness, or evidence of advanced liver disease require admission to an intensive care unit (ICU). Urgent Endoscopy should be performed after adequate resuscitation, usually within 12 hours.
(Ref. CMDT 2010)
6. Acute pancreatitis
Diagnostic tool
1. Severe constant upper abdominal pain may radiate to back relieve by sitting and leaning forwards.
2. Fever & vomiting
3. On exam. – Upper abdominal tenderness but no rigidity and rebound tenderness.

Urgent Investigation
1. S. amylase
2. S. lipase ( if Pt. present after 48 hours)
3. ECG
4. USG of whole abdomen
Management
1. NPO TFO
2. O2 inhalation 4-6 L/ min
3. Infusion Normal saline 1000 cc + 5% DNS 1000 cc i/v @ 20 drops/ min stat and daily
4. Antibiotic-Imipenem (500 mg every 8 hours intravenously) and possibly cefuroxime (1.5 g intravenously three times daily, then 250 mg orally twice daily) administered for no more than 14 days
5. Inj. Omeprazole (40mg) 1 vial i/v stat. & daily
6. Inj. Tramadol HCl (100mg/ml) 1 amp. i.m. stat & 8 hourly
7. NG suction if paralytic illus develops
8. Close monitoring of the pt. with Pulse, BP, and urine out put.
N: B:
• If cause of acute pancreatitis is gall stone then Surgery should be performed after 2 weeks of recovery.
• Oral intake of fluid and foods can be resumed when the patient is largely free of pain and has bowel sounds (even if the serum amylase is still elevated).
(Ref. CMDT 2010 + Oxford American Hand book of critical care.)
7. Chronic pancreatitis
Management:
1. Avoidance of alcohol
2. Analgesia with NSAID or Opiate
3. Oral pancreatic enzyme supplement
4. Dietary fat restriction
5. PPI
6. Coeliac plexus neurolysis or minimally invasive thoracoscopic splaniectomy sometimes required.
(Ref: Davidson)
8. Variceal bleeding
Management:
1. NPO TFO
2. Normal saline 1-2 liter
3. Prophylactic antibiotic – Cephalosporin iv
4. PPI
5. Vasopressor (Terlipressin)-2 mg iv 6 hourly until bleeding stops then 1 mg 6 hourly for further 24 hours
6. Endoscopic procedure to stop variceal bleeding
 Band ligation
-Should be repeated 1-2 week until varices are obliterated. Regular follow up endoscopy is required to identify & treatment of any recurrence of varice.
 Ballon tamponade- Sengstaken-Blakemore tube
7. TIPSS- pt. in whom other treatment is not successful & those with good liver function.
8. Oesophageal transection
– When TIPSS is not available
– Bleeding can not be controlled with other therapies.
9. Portal hypertension
Management:
1. Management of variceal bleeding
2. Primary prevention of variceal bleeding
3. Propanolol 80-160 mg daily or nadalol.( administration of these drugs at doses which reduces heart rate 25% has shown to be effective in primary prevention).
4. Secondary prevention- Beta blocker following banding.

10. Alcoholic liver disease
Management:
1. Cessation of alcohol
2. Nutrition
3. Steroid
Indication:
– Severe alcoholic hepatitis, Maddreys discrimination score >32
Contraindication:
i) Existing sepsis
ii) Variceal haemorrhage
If bilirubin has not fallen 7 days after starting therapy in treatment with steroid, then steroid is unlikely to reduce mortality & should be stopped.
4. Pentoxifylline
5. Use in severe alcoholic hepatitis
6. It appears to reduce incidence of hepato-renal failure
7. Its use is not complicated by sepsis.
5. Liver transplantation

11. NAFLD
Management:
1. Reduce BMI
2. Metformine- 1st line treatment in pt. with DM & NAFLD.
Pioglitazone also improve inflammation & fibrosis.

12. Haemochromatosis
Primary
1. Weekly venesection of 500 ml of blood (250 mg of iron) until S. iron is normal; this may take up to 2 year or more. The aim is to reduce ferittin 1000 µg/ L
Asymptomatic disease is also treated by venesection
4. Screening of HCC by USG

13. Wilson’s disease
Management:
1. Penicillamine –most pt. require 1.5 gm/day (1-4gm/day). The dose can be reduce once the disease is in remission.
Treatment should be continued through out the life including pregnancy. Abrupt discontinuation may precipitate acute liver failure
2. Trientrine dihydrochloride 1.2-2.4 gm/day & Zinc 50 mg 8 hourly, if side effects of penicillin occur.
3. Liver transplantation
– In fulminant liver failure
– Advance cirrhosis with liver failure.
4. Siblings & children of pt. with Wilson’s disease must be investigated & treatment should be given to all affected individual even if they are asymptomatic.

14. Autoimmune Hepatitis
Management:
Prednisolone 40 mg daily
– Dose can be reduced as the pt. & LFT improve. Maintainance therapy is required for at least 2 years after LFT have returned to normal & withdrawl of treatment should not be considered unless liver biopsy is also normal.
– Azathioprine 1-1.5 mg/kg/day allows the dose of prednisolone to be reduced.

15. Primary billiary cirrhosis
Diagnostic tools:
1. Female patient
2. Middle age
3. Flactuating jaundice
4. History of itching.
Asymptomatic
Require monitoring on a yearly basis to assess the onset of symptom & also the disease.
Symptomatic
1. UDCA 13-15 mg/kg/day
2. Liver transplantation if
– Liver failure
– Intractable pruritus
3. Pruritus (Cause- up regulation of opoid receptor & increase endogenous opoid)
Managed by
i) Cholestyramine 4-16gm/day, the powder mixed in orange juice then taken before & after breakfast. It is ineffective in complete billiary obstruction.
ii) Alternative treatment
8. Rifampicin 300 mg/day
9. Naltrexone (opoid antagonist) 25 mg/ day up to 300 mg /day
10. Plasmapheresis
11. Liver support device.
4. Fatigue –no treatmnent , exclude depression & Hypothyroidism
5. Supplementation of fat soluble vitamins
6. Bone disease
Replacement of calcium & vit.D3
Bisphosphonate if evidence of Osteoporesis.

16. Acute cholecystitis
Management:
1. NPO
2. Fluid IV
3. Analgesic-moderate pain-NSAID
4. Severe pain-Pethidine
5. Antibiotic-Cephalosporin (cefuroxime), severely ill add Metronidazple.
6. NG aspiration- if persisting vomiting
7. Surgery should be performed after 6 weeks.

Electrolytes imbalance
1. Ward management of Hyponatraemia
In the ward maximum case of hyponatraemia are hypovoluemic hyponatraemia.
Normal Na+ 135- 145 mmol/L
Hyponatraemia if Na+ 125 mmol/L then oral correction
If Na+ is < 125 mmol/L then iv correction.
 1 TSF table salt contain 96 mmol/L Sodium
 1 L Normal saline contain 154 mmol/L Sodium
 500 ml 3% Sodium contain 512 mmol/L Sodium.

Problem: A pt. present with vomiting followed by unconsciousness. His Na+ is 110 mmol/L. How we will correct his Na+?
Total deficiency = (135 – 110) × 50 × 0.6 mmol/L (His weight is 50 kg).
= 750 mmol/L
Daily correction = 750/3
= 250 mmol/L
So, we have to give 1 L of Normal saline and 1 TSF Table salt daily (approximately) for 3 days.

1. Ward management of Hypenatraemia
Choice of type of fluid for replacement
Hypernatremia with hypovolemia
 Hypovolemic patients should receive isotonic (0.9%) saline to restore the volume deficit and to treat the hyperosmolality.
 After adequate volume resuscitation with normal saline, 0.45% saline or 5% dextrose (or both) can be used to replace any remaining free water deficit.
 Milder volume deficits may be treated with 0.45% saline and 5% dextrose.
Hypernatremia with euvolemia
Water ingestion or intravenous 5% dextrose will result in the excretion of excess sodium in the urine. If the glomerular filtration rate (GFR) is decreased, diuretics will increase urinary sodium excretion.
Hypernatremia with hypervolemia
 Treatment includes 5% dextrose solution to reduce hyperosmolality. Loop diuretics may be necessary to promote natriuresis and lower the total body sodium.
 In severe rare cases with kidney disease, hemodialysis may be necessary to correct the excess total body sodium and water.
3. Treatment of hypocalcaemia
Management:
a) In hyperventilation- rebreathing expired air in a paper bag or administer 5% CO2 in oxygen
b) Inj. 20 ml of 10% solution of Calcium gluconate i.v. slowly stat.
Or
Inj. 20 ml of 10% solution of Calcium gluconate i.m. may be given to obtain a prolonged effect.

4. Treatment of severe hypercalcaemia of malignancy
Management:
1. Rehydration with Normal saline as much as 4-6 L/min. (May need monitoring with CVP in old age or renal impairment)
2. Bisphosphonates e.g. Disodium Pamidronate 90 mg i.v. over 4 hours
3. Additional rapid therapy
a) Forced diuresis with saline & Frusemide
b) Prednisolone 40mg daily
c) Calcitonin
d) Haemodialysis
5. Hypokalaemia
Normal K+ is 3.5-5.5 mmol/L
Hypokalaemia if 2.5 mmol/L.
Intravenous potassium is indicated for patients with severe hypokalemia and for those who cannot take oral supplementation & if K+ is 5.5 mmol/L
Management:
1. iv Calcium gluconate 10 ml of 10 % solution
2. Nebulization with Salbutamol solution
3. iv glucose 50 ml of 50 % (in ward we use 25 % glucose 100 ml) plus inj. Actrapid 5 IU.
These 3 are commonly practiced in the ward. Other treatment options-
1. Inj. Iv Sodium bicarbonate
2. iv Frusemide and Normal Saline
3. Ion –exchange resin (e.g. resonium orally or rectally)
4. Dialysis.

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বাংলাদেশ গর্ভ:

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বাংলাদেশ মোবাইল কোম্পানি

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শাহ হাকিম আখতার দা.বা.

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হাদীস শরীফ

ইসলামিক দুনিয়া

 

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ডাঃ জাকির নায়েক ডঃ জাফর ইকবাল

 

 

 

 

আজ আপনাদের সাথে শেয়ার করব এই দুজনে কিছু বই। বই গুলো আপনাদের জন্য একদম ফ্রি ফ্রি ফ্রি। তারও আবার বাংলায়।।।।

ডাঃ জাকির নায়েক

• সন্ত্রাসবাদ ও জিহাদ-১
• সন্ত্রাসবাদ ও জিহাদ-২
• চাঁদ ও কোরআন
• বিজ্ঞানের আলোকে কোরআন ও বাইবেল
• ইসলাম সম্পর্কে অমুসলিমদের প্রশ্নের জবাব
• ইসলামের উপর অভিয়োগ ও দলিলভিত্তিক জবাব
• বিষয়ভিত্তিক প্রশ্নের জবাব
• ইসলামিক লেভেল
• প্রধান ধর্মসমূহে স্রষ্ঠার ধারণা
• হিন্দুধর্ম ও ইসলাম ধর্ম
• সুদমুক্ত অর্থনীতি
• ইসলাম কি মানবতার সমাধান?
• কেন ইসলাম গ্রহণ করেছি পশ্চিমারা
• কুরআন আধুনিক বিজ্ঞানের বিরুদ্ধে নাকি সাদৃশ্য
• সুন্নাত ও বিজ্ঞান
• সালাত
• ইসলামিক লেভেল
• ইসলাম –ই নারীর অধিকার শিখলে নাকি আধুনিক
• ইসলামের নারী বনাম বই, ইহুদীম খ্রীষ্টান নারী
• ডাঃ জাকির নায়েকের জীবনী

ডঃ জাফর ইকবাল

• Tuk iO Jhayer Dushshahoshik Obhijan
• Zara Biobot
• TratulerJogot
• Titron Ekti Groher Naam
• Swapno
• Suhaner Shopno
• RoboNishi
• Omicronic Rupantar
• Obonil
• Noy Noy Shonno Tin
• Krugo
• Kopotronic Shukh Dukkh
• Ekti Mrittu danda
• Ekjon Otimanobi
• Ikaras
• Eeron
• Jolo manob
• Doler Naam Black Dragon
• Amar Bandhu Rashed
• ChromiumOronnoPart1
• ChromiumOronnoPart2
• BrishtirThikana
• Nishi
• প্রডিজিঃ ডাউনলোড লিঙ্ক।

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সন্তানের হক

সন্তানের হক

সন্তানের হক
আল্লাহ তা‘আলা মানব জীবনকে সন্তান-সন্তুতির মাধ্যমে ভারসাম্যপূর্ণ এবং আকর্ষণীয় করেছেন। পারিবারিক জীবনে সন্তান-সন্ততি কতবড় নিয়ামত তা যার সন্তান হয়নি তিনি সবচেয়ে বেশি উপলব্ধি করে থাকেন। যাদেরকে আল্লাহ রাববুল আলামীন সন্তান দান করেছেন তাদের উপর এক মহান দায়িত্ব অর্পিত হয়েছে। পিতা-মাতার জন্য সবচেয়ে বড় ব্যর্থতা হবে যদি সন্তানকে আদর্শবান রূপে গড়ে না তুলতে পারেন। কেননা আবু হুরায়রা রাদিয়াল্লাহু আনহু থেকে বর্ণিত হাদিসে এসেছে, তিনি বলেন, রাসূলুল্লাহ্‌ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন,

প্রতিটি নবজাতক তার স্বভাবজাত দ্বীন ইসলামের ওপর জন্ম গ্রহণ করে। অতঃপর তার মা-বাবা তাকে ইয়াহূদী, নাসারা অথবা অগ্নিপূজক হিসেবে গড়ে তোলে [সহীহ বুখারী: ১৩৫৮]।
আমাদের সমাজ ব্যবস্থা দিন দিন যেভাবে অপসংস্কৃতি, অনৈতিকতা এবং চরিত্র বিধ্বংসী কাজের দিকে ধাবিত হচ্ছে, সেখানে আমাদের সন্তানের উপর যেসব দায়িত্ব আছে তা অত্যন্ত গুরুত্বের সাথে পালন করতে হবে। আল্লাহ ও তাঁর রাসূলের নির্দেশিত পন্থায় সন্তানকে লালন-পালন করা ঈমানের অন্যতম দাবী। আমাদের উপর সন্তানদের যে হকগুলো রয়েছে তা এখানে আলোচনা করা হলো :
১. কানে আযান দেয়া : সন্তান দুনিয়াতে আসার পর গোসল দিয়ে পরিষ্কার করে তার ডান কানে আযান দেয়া, তা ছেলে হোক বা মেয়ে হোক। এটি পিতা-মাতার উপর এজন্য একটি গুরুত্বপূর্ণ দায়িত্বযে, শিশুর কানে সর্বপ্রথম আল্লাহর শ্রেষ্ঠত্বের আওয়াজ পৌঁছে দেয়া এবং ওত পেতে থাকা শয়তান যাতে তার কোন ক্ষতি না করতে পারে। হাদিসে এসেছে,
আবূ রাফে রাদিয়াল্লাহু আনহু থেকে বর্ণিত, তিনি বলেন, আমি রাসূল সল্লাল্লাহু আলাইহি ওয়াসাল্লামকে হাসান ইবনে আলীর কানে আযান দিতে দেখেছি [সুনান আবূ দাউদ:৫১০৫]
২. সুন্দর নাম রাখা : বাচ্চার জন্য সুন্দর নাম নির্বাচন করা পিতা-মাতার অন্যতম দায়িত্ব ও কর্তব্য। নাম অর্থবহ হওয়া নামের সৌন্দর্য। কেননা রাসূল সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন অনেক অসুন্দর নাম পরিবর্তন করে দিয়েছিলেন। [আবু দাউদ ৪৯৫২-৪৯৬১]
৩. আক্বিকা করা : ইসলামী সংস্কৃতির অন্যতম বিষয় হলো সন্তানের আকীকা করা। ছেলের পক্ষ থেকে ২টি ছাগল এবং মেয়ের পক্ষ থেকে ১টি ছাগল আল্লাহর নামে যবেহ করা। হাদীসে এসেছে,

সামুরা রাদিয়াল্লাহু আনহু হতে বর্ণিত, তিনি বলেন, রাসূলুল্লাহ্ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন, সকল নবজাতক তার আক্বিকার সাথে আবদ্ধ। জন্মের সপ্তম দিন তার পক্ষ থেকে জবেহ করা হবে। ঐ দিন তার নাম রাখা হবে। আর তার মাথার চুল কামানো হবে। [সুনান আবূ দাউদ: ২৮৩৮]
৪. সদকাহ করা : ছেলে হোক বা মেয়ে হোক সপ্তম দিবসে চুল কাটা এবং চুল পরিমাণ রৌপ্য সদকাহ করা সুন্নাত। আলী রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলুল্লাহ সল্লাল্লাহু আলাইহি ওয়াসাল্লাম হাসান রা. এর পক্ষ থেকে ১টি বকরী আকীকা দিয়েছেন এবং বলেছেন, হে ফাতেমা ! তার মাথা মুণ্ডন কর এবং চুল পরিমাণ রৌপ্য সদকাহ কর। [সুনান আত-তিরমিযী: ১৫১৯] এছাড়া রাসূলুল্লাহ্ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম শিশুদেরকে খেজুর দিয়ে তাহনীক এবং বরকতের জন্য দো‘আ করতেন। [সহীহ বুখারী: ৩৯০৯; মুসলিম: ২১৪৬]
৫. খাতনা করা : ছেলেদের খাতনা করানো একটি অন্যতম সুন্নাত। হাদীসে এসেছে,

জাবির রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলুল্লাহ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম হাসান এবং হুসাইন রাদিয়াল্লাহু আনহুমার সপ্তম দিবসে আকীকা এবং খাতনা করিয়েছেন। [আল-মু‘জামুল আওসাত: ৬৭০৮]
৬. তাওহীদ শিক্ষা দেয়া : শিশু যখন কথা বলা আরম্ভ করবে তখন থেকেই আল্লাহর তাওহীদ শিক্ষা দতে হবে। রাসূলুল্লাহ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম ইবন আব্বাস রাদিয়াল্লাহু আনহুকে লক্ষ্য করে বলেন,
‘

হে বৎস! আমি তোমাকে কয়েকটি বাক্য শিখাতে চাই। তুমি আল্লাহর অধিকারের হেফাযত করবে, আল্লাহও তোমার হেফাযত করবেন। তুমি আল্লাহর অধিকারের হেফাযত করবে, তুমি তাঁকে সর্বদা সামনে পাবে। যখন কোন কিছু চাইবে তখন আল্লাহর কাছেই চাইবে। আর যখন সহযোগিতা চাইবে তখন আল্লাহর কাছেই চাইবে। আর জেনে রাখ! যদি পুরো জাতি যদি তোমার কোন উপকার করার জন্য একতাবদ্ধ হয়, তবে তোমার কোন উপকার করতে সমর্থ হবে না, শুধু ততটুকুই করতে পারবে যতটুকু আল্লাহ তোমার জন্য লিখে রেখেছেন। আর যদি পুরো জাতি যদি তোমার কোন ক্ষতি করার জন্য একতাবদ্ধ হয়, তবে তোমার কোন ক্ষতি করতে সমর্থ হবে না, শুধু ততটুকুই করতে পারবে যতটুকু আল্লাহ তোমার জন্য লিখে রেখেছেন। কলমের লিখা শেষ হয়েছে এবং কাগজসমূহ শুকিয়ে গেছে। [তিরমিযী: ২৫১৬]
৭. কুরআন শিক্ষা দান : ছোট বেলা থেকেই সন্তানকে কুরআন শিক্ষা দিতে হবে। কেননা কুরআন শিক্ষা করা ফরয। আলী রাদিয়াল্লাহু আনহু থেকে বর্ণিত, তিনি বলেন, তোমরা তোমাদের সন্তানদের তিনটি বিষয় শিক্ষা দাও। তন্মধ্যে রয়েছে তাদেরকে কুরআন তিলাওয়াত শিক্ষা ও কুরআনের জ্ঞান দাও। [জামিউল কাবীর]
কুরআন শিক্ষা দেয়ার চেয়ে উত্তম কাজ আর নেই। উসমান রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলুল্লাহ সল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন:

‘‘তোমাদের মধ্যে সর্বোত্তম ব্যক্তি সেই যে নিজে কুরআন শিক্ষা করে ও অপরকে শিক্ষা দেয়।’’ [সহীহ বুখারী:৫০২৭]
৮. সলাত শিক্ষা দেয়া ও সলাত আদায়ে অভ্যস্ত করা : এটি একটি গুরুত্বপূর্ণ অধিকার যে পিতা-মাতা তার সন্তানকে সলাত শিক্ষা দিবেন এবং সলাত আদায়ে অভ্যস্ত করাবেন। হাদীসে এসেছে,

আমর ইবনে শূয়াইব রাদিয়াল্লাহু আনহু তার বাবা তিনি তার দাদা থেকে বর্ণনা করেন, নবী সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম ইরশাদ করেন, তোমরা তোমাদের সন্তানদের সলাতের নির্দেশ দাও সাত বছর বয়সে। আর দশ বছর বয়সে সলাতের জন্য মৃদু প্রহার কর এবং শোয়ার স্থানে ভিন্নতা আনো। [সুনান আবূ দাউদ: ৪৯৫]
৯. আদব বা শিষ্টাচার শিক্ষা দেয়া : সন্তানদের আচরণ শিক্ষা দেয়া পিতামাতার উপর দায়িত্ব ও কর্তব্যের অন্তর্ভূক্ত। লুকমান আলাইহিস সালাম তার সন্তানকে বললেন, ‘আর তুমি মানুষের দিক থেকে তোমার মুখ ফিরিয়ে নিয়ো না। আর যমীনে দম্ভভরে চলাফেরা করো না; নিশ্চয় আল্লাহ কোন দাম্ভিক, অহঙ্কারীকে পছন্দ করেন না। আর তোমার চলার ক্ষেত্রে মধ্যমপন্থা অবলম্বন কর, তোমার আওয়াজ নীচু কর; নিশ্চয় সবচাইতে নিকৃষ্ট আওয়াজ হল গাধার আওয়াজ।’ [ সূরা লুকমান ১৮,১৯]
১০.আদর স্নেহ ও ভালবাসা দেয়া : সন্তানদেরকে স্নেহ করা এবং তাদেরকে আন্তরিকভাবে ভালবাসতে হবে। আবু হুরায়রা রাদিয়াল্লাহু আনহু থেকে বর্ণিত, তিনি বলেন, রাসূলুল্লাহ্‌ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম হাসান ইবনে আলী রাদিয়াল্লাহু আনহুকে চুম্বন দিলেন এবং আদর করলেন। সে সময় আকরা ইবনে হাবিস রাদিয়াল্লাহু আনহুও উপস্থিত ছিলেন। তিনি বলতে লাগলেন, আমারতো দশটি সন্তান কিন্তু আমিতো কখনো আমার সন্তানদেরকে আদর স্নেহ করিনি। রাসূলুল্লাহ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম তার দিকে তাকালেন এবং বললেন, যে অন্যের প্রতি রহম করে না আল্লাহও তার প্রতি রহম করেন না। [সহীহ বুখারী: ৫৯৯৭]
১১. দ্বীনি ইলম শিক্ষা দেয়া : সন্তানকে দীনি ইলম শিক্ষা দেয়া ফরজ করা হয়েছে। কারণ দ্বীনি ইলম না জানা থাকলে সে বিভ্রান্ত এবং ক্ষতিগ্রস্থদের অন্তর্ভূক্ত হবে। হাদীসে এসেছে-

আনাস বিন মালিক রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলুল্লাহ সল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন, প্রত্যেক মুসলিমের উপর জ্ঞানার্জন করা ফরয। [সুনান ইবন মাজাহ: ২২৪]
১২. প্রাপ্ত বয়স্ক হওয়া পর্যন্ত লালন-পালন করা : সন্তানদেরকে প্রাপ্ত বয়স্ক পর্যন্ত লালন-পালন করতে হবে এবং তাদের জন্য প্রয়োজনীয় খরচ করতে হবে।

উম্মে সালামাহ রাদিয়াল্লাহু আনহা থেকে বর্ণিত, তিনি বলেন, নবী সাল্লাল্লাহু আলাইহি ওয়াসাল্লামকে আমি জিজ্ঞাসা করলাম আবূ সালামার সন্তানদের জন্য আমি যদি খরচ করি এতে কি আমার জন্য প্রতিদান রয়েছে? নবী সল্লাল্লাহু আলাইহি ওয়াসাল্লাম বললেন, হ্যাঁ যতদিন তুমি খরচ করবে ততদিন তোমার জন্য প্রতিদান থাকবে। [সহীহ বুখারী: ৫৩৬৯]
১৩. সক্ষম করে তোলা : সন্তানদেরকে এমনভাবে সক্ষম করে গড়ে তোলা,তারা যেন উপার্জন করার মত যোগ্যতা অর্জন করতে পারে। সা‘দ ইবনে আবি ওয়াক্কাস রাদিয়াল্লাহু আনহু থেকে বর্ণিত, তিনি বলেন, নবী সাল্লাল্লাহু আলাইহি ওয়া সাল্লাম আমাকে এভাবে বলেছেন,

তোমাদের সন্তান সন্ততিদেরকে সক্ষম ও সাবলম্বি রেখে যাওয়া, তাদেরকে অভাবী ও মানুষের কাছে হাত পাতা অবস্থায় রেখে যাওয়ার চেয়ে উত্তম। [সহীহ বুখারী:১২৯৫]
১৪. বিবাহ দেয়া : সুন্নাহ পদ্ধতিতে বিবাহ দেয়া এবং বিবাহর যাবতীয় কাজ সম্পাদন করা এবং উপযুক্ত সময়ে বিবাহর ব্যবস্থা করা। আবূ হুরায়রা রাদিয়াল্লাহু আনহু থেকে এভাবে বর্ণনা করা হয়েছে যে, নিশ্চয়ই পিতার উপর সন্তানের হকের মধ্যে রয়েছে, সন্তান প্রাপ্তবয়স্ক হলে তাকে বিবাহ দেবে। [জামিউল কাবীর]
১৫. দ্বীনের পথে পরিচালিত করা : পিতা-মাতার অন্যতম দায়িত্ব হলো সন্তানদেরকে দ্বীনের পথে, কুরআন-সুন্নাহর পথে পরিচালনা করা, দ্বীনের বিধান পালনের ক্ষেত্রে অভ্যস্ত করে তোলা। কুরআনে এসেছে,

‘ বল, ‘এটা আমার পথ। আমি জেনে-বুঝে আল্লাহর দিকে দাওয়াত দেই এবং যারা আমার অনুসরণ করেছে তারাও। আর আল্লাহ পবিত্র মহান এবং আমি মুশরিকদের অন্তর্ভূক্ত নই’। [সূরা ইউসুফ : ১০৮]
সন্তানকে দ্বীনের পথে পরিচালনার মাধ্যমে সওয়াব অর্জন করার এক বিরাট সুযোগ রয়েছে। হাদীসে এসেছে, রাসূলুল্লাহ্‌ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম আলী রাদিয়াল্লাহু আনহুকে বললেন,

তোমার মাধ্যমে একজনও যদি হিদায়াতপ্রাপ্ত হয়, তবে তা হবে তোমার জন্য লালবর্ণের অতি মূল্যবান উট থেকেও উত্তম। [সহীহ বুখারী]
১৬. সন্তানদের মাঝে ইনসাফ করা : সন্তানগণ পিতামাতার কাছ থেকে ইনসাফ আশা করে এবং তাদের মাঝে ইনসাফ করা একটি গুরুত্বপূর্ণ বিষয়। রাসূলুল্লাহ্‌ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম এ বিষয়ে বিশেষভাবে সতর্ক করে বলেছেন, ‘তোমরা আল্লাহকে ভয় করো এবং তোমাদের সন্তাদের মাঝে ইনসাফ করো’। [সহীহ বুখারী: ২৫৮৭]
১৭. ইসলাম অনুমোদন করে না এমন কাজ থেকে বিরত রাখা : ইসলাম অনুমোদন করে না এমন কাজ থেকে তাদেরকে বিরত না রাখলে এই সন্তানগনই কিয়ামাতে পিতামাতার বিরুদ্ধে দাঁড়াবে। কুরআনে এসেছে,

হে ইমানদারগণ! তোমরা তোমাদের নিজেদেরকে এবং তোমাদের পরিবারবর্গকে জাহান্নামের আগুন থেকে বাঁচাও। [সূরা আত-তাহরীম-৬]

আর কাফিররা বলবে, ‘হে আমাদের রব, জ্বিন ও মানুষের মধ্যে যারা আমাদেরকে পথভ্রষ্ট করেছে তাদেরকে আমাদের দেখিয়ে দিন। আমরা তাদের উভয়কে আমাদের পায়ের নীচে রাখব, যাতে তারা নিকৃষ্টদের অন্তর্ভুক্ত হয়। [সূরা হা-মীম আসসিজদাহ-২৯ ]
১৮. পাপকাজ, অশ্লিলতা, বেহায়াপনা, অপসংস্কৃতি থেকে বিরত রাখা : সন্তান দুনিয়ার আসার সাথে সাথে শয়তান তার পেছনে লেগে যায় এবং বিভিন্নভাবে, ভিন্ন ভিন্ন রুপে,পোশাক-পরিচ্ছেদের মাধ্যমে, বিভিন্ন ফ্যাশনে, বিভিন্ন ডিজাইনে, বিভিন্ন শিক্ষার নামে জাহান্নামের দিকে নিয়ে যাওয়ার ষড়যন্ত্র করে। তাই পিতা-মাতাকে অবশ্যই এ বিষয়ে সতর্ক ও সজাগ থাকতে হবে। আল্লাহ বলেন,

হে মুমিনগণ, তোমাদের স্বামী-স্ত্রী ও সন্তান-সন্ততিদের কেউ কেউ তোমাদের দুশমন। অতএব তোমরা তাদের ব্যাপারে সতর্কতা অবলম্বন কর। আর যদি তোমরা মার্জনা কর, এড়িয়ে যাও এবং মাফ করে দাও তবে নিশ্চয় আল্লাহ পরম ক্ষমাশীল, অসীম দয়ালু। [সূরা তাগাবুন-১৪]
হাদীসে এসেছে,

ইবনে আববাস রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলে করীম রাসূলুল্লাহ সল্লাল্লাহু আলাইহি ওয়াসাল্লাম পুরুষের বেশ ধারণকারী নারী ও নারীর বেশ ধারণকারী পুরুষকে অভিসম্পাত করেছেন। [সহীহ বুখারী:৫৮৮৫]
আব্দুল্লাহ ইবন আমর রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলুল্লাহ্ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন :

‘যে ব্যক্তি অন্য জাতির সাথে সা-দৃশ্যতা রাখবে সে তাদের দলভুক্ত বলে গণ্য হবে। [সুনান আবূ দাউদ:৪০৩১]
১৯. দো‘আ করা : আমাদের সন্তানদের জন্য দো‘আ করতে হবে। আল্লাহ তা‘আলা আমাদেরকে দো‘আ শিক্ষা দিয়েছেন এভাবে,

আল্লাহর নেক বান্দা তারাই যারা বলে, হে আমাদের রব, আমাদেরকে এমন স্ত্রী ও সন্তানাদি দান করুন যারা আমাদের চক্ষু শীতল করবে। আর আপনি আমাদেরকে মুত্তাকীদের নেতা বানিয়ে দিন। [সূরা আলফুরকান-৭৪]
যাকারিয়্যা আলাইহিস সালাম আল্লাহর নিকট দো‘আ করেছিলেন,

‘হে আমার রব, আমাকে আপনার পক্ষ থেকে উত্তম সন্তান দান করুন। নিশ্চয় আপনি প্রার্থনা শ্রবণকারী’। [সূরা আলে ইমরান ৩৮]
সম্মানিত পিতামাতাবৃন্দ, আমরা কি সন্তানের হকগুলো পালন করতে পেরেছি বা পারছি ? আসুন, আমরা আমাদের সন্তানদেরকে নেকসন্তান হিসাবে গড়ে তুলি। যে সম্পর্কে হাদিসে এসেছে,

আবু হুরায়রা রাদিয়াল্লাহু আনহু থেকে বর্ণিত, রাসূলুল্লাহ সাল্লাল্লাহু আলাইহি ওয়াসাল্লাম বলেছেন, মানুষ মৃত্যুবরণ করলে তার যাবতীয় আমল বন্ধ হয়ে যায়, তবে ৩ টি আমল বন্ধ হয় না-
১. সদকায়ে জারিয়া
২. এমন জ্ঞান-যার দ্বারা উপকৃত হওয়া যায়
৩. এমন নেক সন্তান- যে তার জন্য দো‘আ করে [সহিহ মুসলিম:১৬৩১]
আল্লাহ তা‘আলা আমাদের সন্তানদেরকে কবুল করুন,
তাদের হকসমূহ যথাযথভাবে পালন করার তাওফীক দিন। আমীন!
হাবীবুল্লাহ মুহাম্মাদ ইকবাল
সম্পাদনা : ড. আবু বকর মুহাম্মাদ যাকারিয়া

SSC Result 2011 will be published after 2:00pm on 12.05.2011

SSC Result 2011 will be published after 2:00pm on 12.05.2011
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Bone Anatomy

Bone Anatomy

www.armsekram.com

 

 

Introduction:

There are lots of clinical symptoms in elderly patient’s. Among these problems, low back pain is one of the most common and agonizing symptoms, some times that becomes a chronic one. Back pain is considered chronic when there is no relief after months of pain, which requires an accurate diagnosis to determine the treatment that is most likely to help.¹

The skeleton is not only an adaptable and well articulated frame, but also a dynamic mineral reserve bank in which the body stores its calcium and phosphorus in a metabolically stable and structurally useful way. In 1993 experts of osteoporosis consensus development conference in Hong Kong define osteoporosis as a metabolic disease characterized by low bone mass and micro architectural deterioration of bone tissue leading to enhanced bone fragility and consequent increase in fracture risk.² The World Health Organization (WHO) defines osteoporosis as a bone density more than 2.5 standard deviation (SDs) below the young adult mean value (T-score < – 2.5). Values between 1 & 2.5 SDs below the young adult mean are termed “osteopenia”.³

In normal individuals bone mass increases during skeletal growth to reach a peak between the ages of 20 and 25 but fall there after in both sexes.⁴ Increased sex hormone production at puberty is required for skeletal maturation, which reaches maximum mass and density in early adulthood. Nutrition and life style also play an important role in growth, though genetic factors are the major determinants of peak skeletal mass and density. Peak bone mass is often lower among individuals with a family history of osteoporosis. After the age of 30 to 45, however the resorption and formation process become imbalanced, and resorption exceeds formation.⁵

Aging is a natural process. Osteoporosis is a major age related disease. Menopause is associated with decline in ovarian production of estrogen. Trabecular or cortical bone loss accelerates in women after natural menopause.

In most cases, osteoporosis remaining a silent disease, until a fracture of femur or lumber vertebra occurs. Its mains clinical significance lies in the predisposition to fracture, particularly of the wrist, vertebra, and proximal femur. It is well known that the development of one osteoporotic fracture markedly increases the relative risk of a second fracture as much as 20 folds.⁷

As the risk of fracture increases exponentially with age, changing population demographics will increase the burden of disease (currently costing almost 1 billion pound annually in the U.K.). The lifetime risk of hip fracture for white women at age 50 is around 15%, 5% for men, with equal risk around 11-13% for colles’ or vertebral fracture. Of those surviving to 80 years of age, 30% of women and 15% of men will suffer hip fracture.³

Bone strength is closely correlated with bone mineral density (BMD). In recent years, Prospective study have been shown that BMD can predict fracture risk more early than any other conventional investigating modalities.⁸ It is not possible to learn how strong or weak ones bone are from a blood test or a risk factor quantification. The only way to determine osteoporotic changes in the skeleton is to measure bone density directly, for which Dual energy X-ray absorptiometry (DEXA) bone mineral densitometry is very much useful non-invasive method.⁹

The prevalence of osteoporosis seems daunting, and the consequences, especially in elderly peoples, appear inevitable, it is still not a high enough health care priority in developing countries like Bangladesh.

The present study was conducted among the elderly patient’s admitted with low back pain to evaluate the frequency of osteoporotic changes in skeleton, and the associated risk factors which could have bearings in prevention and reduction of morbidity & mortality of osteoporosis in Bangladesh.

 

 

 

BONE ANATOMY AND PHYSIOLOGY  

 

Normal skeletal system:

The skeletal system is a vital to life as any organ system because it plays an essential role in mineral homeostasis, houses hematopoietic elements, provides mechanical support for movement, and protects and determines the attributes of body size and shape. The skeletal system is composed of 206 bones that vary in size and shape (trabecular, flat, cuboid), and this diversity is an example of how form reflects function. The bones are interconnected by a variety of joints that allow for a wide range of movement while maintaining stability. ¹⁰

 

Bone embryology-

The skeletal system develops from mesenchyme, which is derived from the mesodermal germ layer and from neural crest. Some bones, such as the flat bones of the skull, undergo membranous ossification: that is mesenchyme cells are directly transformed in to osteoblast. In most bones, such as the long bones of the limbs, mesenchyme condenses and form hyaline cartilage models of bones. Ossification centers appear in these cartilage models, and bone gradually ossifies by endochondrial ossification.

The skull consists of the neurocranium and viscero cranium (face). The neurocranium includes a membranaous portion, which forms the cranial vault, and cartilaginous portion (chondrocranium), which form the base of the skull. Neural crest cell from the face, most of the cranial vault, and prechordal part of the chondrocranium (the part that lies rostal to the notochord). Paraxial mesoderm form the remainder of the skull.

Limbs form as buds, along the body wall that appear in the fourth weak Lateral plate mesoderm forms the bones and connective tissue, while muscle cell migrate to the limbs from the somites of the AER regulates limbs out growth and ZPA controls antero posterior patterning.

The vertebral column and ribs develop from the sclerotome compartment of the somites, and the sternum is derived form mesoderm in the ventral body wall. A definitive vertibra is formed by condensation of the caudal half of one sclerotome and fusion with the cranial half of the subjacent sclerotome.¹¹

In endochondral ossification , in which an initial cartilage template is invaded by vascular tissue containing osteoprogenitor cells. The cartilage in them replaced by bone that extends from the centers of ossification situated in the middle and ends of the developing bone. A thin remnant of cartilage remains at each end of the bone during child hood, and is referred to as the growth plate or epiphysis. Growth depends on division of chondrocytes with in the epiphysis. Cell division takes place in the proliferative zone nearest the end of the long bone, and newly formed chondrocytes migrate downwards and enlarge in the hypertropic zone, chondrocyte death ensues and surrounding matrix calcifies before being removed and replaced by mature bone. During puberty, the rise in circulating levels of sex hormones halts cell division in growth plate. The cartilage remnant then disappears as the epiphysis fuse, and longitudinal bone growth ceases. ⁴

Bone Anatomy & Histology-

Bone is a type of vascularized dense connective tissue with cell embedded in a matrix composed of organic material, mainly collagen fibers, and inorganic salt rich in calcium & phosphate.¹²

Types of bone-

Gross observation of bone in cross section shows dense areas without cavity-corresponding to compact bone and areas with numerous interconnecting cavities corresponding to cancellous (spongy) bone. Under microscope, however both compact bone and trabeculae separating the cavites of cancellous bone have the same basic histologic structure.

In long bone, the bulbous end called epiphysis, are composed of spongy bone covered by a thin layer of compact bone. The cylindrical part- diaphysis is almost totally composed of compact bone, with a small component of spongy bone on its inner surface around the bone marrow cavity. Short bones usually have a core of spongy bone completely surrounded by compact bone. The flat bone that form the calvaria have two layers of compact bone called plates (table), separated by layer of spongy bone called the diploe. ¹³  Cortical bone constitute roughly 80% of the adult skeleton and predominates in the shaft of the long bone. ¹⁴

Microscopic examination of bone shows two varieties: primary, immature, or woven bone and secondary, mature or lamellar bone. Primary bone is the first bone tissue to appear in embryonic development and in fracture repair and other repair processed, it is characterized by random deposition of tissue collagen fibers, in contrast to the organized lamellar deposition of collagen in secondary bone.

Primary bone tissue –

Primary bone tissue is usually temporary and is replaced in adults by secondary bone tissue except in a very few places in the body. e.g. near the suture of the flat bones of the skull, in tooth sockets and in the insersion of some tendons.

Secondary bone tissue –

Secondary bone tissue is the variety usually found in adult. It characteristically shows collagen fibers arranged in lamellae. The whole complex of concentric lamellae of bone surroundings a canal containing blood vessels, nerves and loose connective tissue is called Haversian system or osteon. In compact bone lamellae exhibit outer circumferential lamellae.

Each Haversian system is a long, often bifurcated cylinder parallel to the long axis of the disphysis. It consists of a central canal surrounded by 4-22 concentric lamellae. The Haversian canals communicate with the marrow cavity, the periosteum and one another through transverse or oblique Volkmann’s canal. Volkmann’s canals do not have concentric lamellae; instead, they perforate the lamellae. ¹³

Bone marrow-

The medullary cavity in long bones and the interstices of cancellous bone are filled with red or yellow marrow. At birth all the marrow of all the bones is red, active haemopoiesis is going on every where. As age advanced the red marrow atrophies and is replaced by yellow, fatty marrow with no power of haemopoiesis. This change begins in the distal parts of the limbs and gradually progresses proximally. By young adult life there is little red marrow remaining in the limb bones, and that only in their cancellous ends; ribs, sternum, vertebrae and skull bones contain red marrow throughout life.¹²

Periosteum & endosteum-

 

The outer surface of the bones is covered with a thick layer of vascular fibrous tissue. This layer is the periosteum and nutrition of the underlying bone substance depends on the integrity of its blood vessels. The periosteum is osteogenic, its deeper cell differentiating into osteoblast when required. In the growing individual new bone is laid down under the periosteum, and even after growth has ceased the periosteum retains the power to produce new bone when it is needed. eg. in the repair of fracture. The periosteum is united to the underlying bone by collagen (Sharpey’s) fibers, particularly strongly over the attachment of the tendon and ligaments. Periosteum does not, of course, cover the articulating surface of the bones in synovial joints, it is reflected from the articular margins to join the capsule of the joint. The single layered endosteum that lines inner bone surface (marrow cavity and vascular canals) is also osteogenic and contributes to new bone formation.⁴

Composition of bone –

Cellular component – bone is composed of cellular and non cellular components. The three most specialized cell types necessary for metabolic activities of bone are osteoblasts, osteoclasts and osteocytes. ¹⁴

Osteoblasts – are derived from pleuripotential bone marrow stem cells that are capable of differentiation into fibroblastic, adipocytic, or chondrocytic / osteoblastic lineages. A critical signal for osteoblastic differentiation is provided by expression of the transcription factor cbfa-1. When dormant osteoblasts  ( bone-lining cell) on the bone surface are activated to mature osteoblasts, they synthesize uncalcified bone matrix, or osteoid, and then  promote its subsequent mineralization. Osteoblasts express specific receptor  for parathyroid hormone (PTH), 1, 25 – dihydroxy vitamin D (1,25 [OH]₂ D), insulin like growth factor 1, insulin, interleukin-1, interleukin-6, interleukin-11, thyroid hormone, estrogen, androgen, and glucocorticoids.¹⁴ Some osteoblasts  are gradually surrounded by newly formed matrix and become osteocyte. During this process a space called lacuna is formed. Lacunae are occupied by osteocytes and their extension. ¹³

Osteocytes – Osteocytes which derive from osteoblasts, lie in the lacunae situated between lamellae of matrix. Only one osteocyte is found in each lacuna.⁵  They communicate with each other and surface cells via an intricate network of tunnels through the matrix known as canaliculi. The osteocytic cell processes traverse the canaliculi, and their contracts along gap junctions allow the transfer of surface membrane potentials and substrates. The large number of osteocytic processes and their distribution through out bone tissue enable them to be the prime cell in several biological processes. Osteocytes  also have the capability to detect mechanical forces and translate them in to biologic activity, including the release of chemical mediators by signal transduction pathways involving cyclic adenosine monophosphate.¹⁵

Osteoclasts – The osteoclast is the cell responsible for bone resorption is derived from haematopoietic progenitor cell that also give rise to monocytes and macrophages. Cytokines crucial for osteoclast differentiation and maturation include interleukin (IL)-1, IL-3, IL-6, IL-11, tumor necrosis factor (TNF), granulocyte – macrophage colony stimulation factor (GM-CSF), and macrophage colony stimulating factor (M-CSF).¹⁶  Osteoclasts and their progenitors appear to lack receptor for PTH, various cytokines, vitamin D, and other hormones that regulate osteoclastogenesis.¹⁷ Osteoclast are very large, branched motile cells.  Dilated portion of the cell body contain from 5 to 50 (or more) nuclei. In areas of bone undergoing resorption, osteoclasts lie within Howship’s lacunae. In active osteoclasts, the surface facing bone matrix is folded in to irregular often subdivided projections, forming a ruffled border. Surrounding the ruffled border is a cytoplasmic zone –  the clear zone that is devoid of organelles, yet rich in actin microfilaments. This zone is a site of adhesion of osteoclast to the bone matrix and creates a micro environment in which bone resorption occurs. The osteoclast secretes collagenase and other enzymes and pumps protons in to a sub cellular pocket, promoting the localized digestion of collagen and dissolving calcium salt crystals. ¹⁸

Non cellular components :- The non cellular components of bone include the organic matrix and inorganic matrix, which comprise roughly one third and two third respectively of total bone mass.¹⁴  The organic matter is mainly protein.¹⁹ Type -1  collagen, the most abundant structural protein in bone, make up 90% of the organic matrix. Other proteins in bone include small amounts of other collagens and a host of non collagenous proteins, including osteonectin, osteocalcin, osteopontin, fibronectin, thrombospondin, bone sialo protein, proteoglycans, and serum protein.²⁰ The non collagenous protein of bone are bound to the matrix and grouped according to their functions as adhesion protein, calcium binding proteins, mineralization proteins, enzymes, cytokines, and growth factors.²¹ Of these only osteocalcin is unique to bone. It is measurable in the serum and used as a sensitive and specific marker for osteoblast activity.²² Osteonectin, a bone specific protein linking mineral to collagen.²³   Inorganic matter represent about 50% of the dry weight of bone matrix. Calcium and phosphorus are especially abundant, but bicarbonate, citrate, magnesium, potassium, and sodium are also found. Calcium and phosphorus form hydroxyapatite crystals with the composition Ca₁₀ (PO₄)₆(OH)₂. Significant quantities of amorphous (non crystalline) calcium phosphate are also present. In electron micrographs, hydroxyapatite crystals of bone appear as pales that lie along side the collagen fibrils but are surrounded by ground substance. The surface ions of hydroxyapatite are hydrated, and a layer of water and ions forms around the crystal. This layer , the hydration shell, facilitates the exchange of ions between the crystal and the body fluid.²⁴

Bone modeling and remodeling: – Osteoblasts and osteoclasts act in coordination and are considered the functional unit of bone known as the basic multicellular unit. The process of bone formation and resorption are tightly coupled, and their balance determine skeletal mass at any point in time.¹⁶  Throughout the life, bone is being constantly reabsorbed and new bone is being formed. The calcium in bone turns over at a rate of 100% per year in infants and 18% per year in adults. About 5% of bone mass is being remodeled in human skeleton at any one time. The renewal rate for bone is about 4% per year for compact bone and 20% per year for trabecular bone.²⁵ In the formation and maintenance of skeletal system, osteoblast provides much of the local control because it not only produce bone matrix, but also plays an important role in mediating osteoclast activity. Many of the primary stimulators of the bone resorption, such as parathyroid hormone, parathyroid hormone- related protein (PHRP), IL-1 and TNF have minimal or no direct effect on osteoclast. The osteoblast has receptors for these substances, and evidence suggests that once the osteoblast receives the appropriate signals it release a soluble mediator that induces osteoclast bone resorption. The cytokine and growth factor, especially TGF-β, released from the matrix during its digestion act as a feedback loop and trigger the formation and activation of osteoblast to synthesize and deposit an equivalent amount of new bone in the resorption pit¹. Osteoclast mediated resorption of bone takes place in scalloped spaces ( Howship’s lacunae) where the osteoclasts are attached through a specific α_v β₃ integrin to components of the bone matrix such as osteopontin. The osteoclast form a tight seal to the underlining matrix and secrets protons, chloride, and proteinases in to a confined space linked to an extra cellular lysosome. The active osteoclast surface forms a ruffled border that contains a specialized proton-pump ATPase, which secretes acid and solubilizes the mineral phase. Carbonic anhydrase with in the osteoclast generates the needed protons. The bone matrix is reabsorbed in the acid environment adjacent to the ruffled border by proteases that act as low P^H,  such as cathepsin-k.

New bone, whether formed in infants or in adult during repair, has relatively high ratio of cell to matrix and is characterized by coarse fiber bundle of collagen that are interlaced and randomly dispersed (woven bone). In adult, the more mature bone is organized with fiber bundles regularly arranged in parallel or concentric sheets (lamellar bone). In long bones, deposition of lamellar bone in a concentric arrangement around blood vessels forms the Haversian system. The growth in length of bones is dependent on proliferation of cartilage cells and on the endochondrial sequence at the growth plate. Growth in width and thickness is accomplished by formation of bone at the periosteal surface and by resorption at the endosteal surface, with the rate of formation exceeding that of resorption. In adult, after the growth plate close, growth in length and endochondral bone formation cease, except for some activity in the cartilage cells beneath the articular surface.

Remodeling of bone occurs along lines of force generated by mechanical stress. This signal from these mechanical stresses is sensed by osteocytes, which transmit signals to osteoclasts or osteoblast or their precursors. A bowing deformity increase new bone formation at concave surface and resorption at convex surface, seemingly designed to produce the strongest mechanical structure. Bone plasticity reflects the interaction of cells with each other and with the environment. The product of osteoblast and osteoclast activity can assist in the diagnosis and management of bone disease. Osteoblast activity can be assessed by measuring serum bone specific alkaline phosphatase.  Similarly, osteocalcin, a protein secreted from osteoblast, is made virtually only by osteoblast. Osteoclast, activity can be assessed by measurement of products of collagen degradation.

The cycle of bone remodeling is carried out by the basic multicellular unit (BMU), comprising a group of osteoclasts and osteoblasts. In cortical bone , the BMUs tunnel through the tissue, where as in cancellous bone, they move across the trabecular surface. The process of bone remodeling is initiated by contraction of the lining cell and recruitment of osteoclast precursors. These precursors fuse to form multinucleated, active osteoplast that mediate bone resorption. Osteoclast adheres to bone and subsequently remove it by acidification and proteolytic digestion. As the BMU advances, osteoclast leave the resorption site and osteoblast move into cover the excavated area and begin the process of new bone formation by secreting osteoid, which is eventually mineralized in to new bone. After osteoid mineralization, osteoblast flatten and form a layer of lining cells over new bone.⁵. On completing the cycle (about 120 days), remodeling is balanced if there has been no net change in the amount of bone.³

Blood and nerve supply of the bone:-

One or two nutrient arteries enter the shaft of a long bone obliquely and usually directed away from the growing end. Within the medullary cavity they divided into ascending and descending branches. Near the ends of bone, they are joined by branches from the neighboring systemic vessels and from periarticular vascular arcades. Cortical bone receives blood supply from periosteum and from muscular vessels at their attachment. Vein are numerous and large in the cancellous red marrow bone (e.g. the basi vertebral veins) Lymphatics are present, but scanty; they drain to the regional lymph nodes of the part.

Subcutaneous periosteum is supplied by the nerves of the overlying skin. In deeper parts of the local nerves, usually the branches to nearby muscle provide the supply. Periosteum in all parts of the body is very sensitive. Other nerves, probably vasomotor in function, accompany nutrient vessels into bone.

 

Peak bone mass:-

Peak bone mass (PBM) can be defined as the amount of bony tissue present at the end of the skeletal maturation. The precise age at which peak bone mineral density is a acquired is still unknown and may be site dependent. In general, accepte that up to 90% of peak bone mass is acquired by age 18 in girl and by age 20 in boys, which makes youth the best time to invest in bone health. There after, bone mass increase slightly during the third decade of life and reaches its peak around age 30 years. So, peak bone mass is achieved during adulthood. Its magnitude is determined largely by hereditary factors, especially the allele for the vitamin D receptor molecule. Physical activity, muscle strength, diet, and hormone state however all contribute.²⁶. Factors that may affect peak bone mass- sex, race, genetic factors, gonadal steroids, growth hormone, timing of puberty, calcium intake, exercise, etc.¹⁴

Sex and race: White woman have lighter skeletons, than white man or black women, where as black men have the heaviest skeleton.²⁷ The skeleton of Asians appear to be intermediate between those of blacks and whites. In all the three races, women have lower peak bone mass than men. Because initial bone mass is an important determinant of bone mass latter of life, these difference may partially explain observed racial and sexual difference in the incidence of osteoporoses and fractures. However, such generalization should not obscure the fact that some white have high   bone mass, where as individual non-whites may have low bone mass and fracture. Moreover, there seem to be exceptions to the general pattern: Hispanics appear to have hip fracture rate that are even lower than American black. Whereas the Bantu people of South Africa have extremely low fracture rate but also low bone mass. ²⁸

 

Genetic factors: The impact of genetic factors on bone density has been demonstrated in several ways. For example, bone density is lower in daughters of women with osteoporosis than in the daughters of women without osteoporosis. Moreover, the concordance of bone density is much higher among monozygotic twins than dizygotic twins.²⁹ Several genes, including the vitamin D receptor gene, the genes encoding type-1 procollagen, and the estrogen receptor gene, have been implicated in the pathogenesis of osteoporosis, but no conclusive genetic linkages have been demonstrated.¹⁴ The type of vitamin D receptor molecule that is inherited accounts for approximately 75% of the maximal peak mass achieved. Polymorphism in the vitamin D receptor or molecule is associated with either a highest or lower maximal bone mass.

Nutrition: Calcium is essential for healthy bone development, and increasing the calcium intake in children and adolescent increase bone growth. Calcium deficiency in young people can account for a 5 to 10 percent different in peak bone mass and can increase the risk for hip fracture latter in life. The skeleton appears to be more responsive to calcium supplementation before the onset of puberty than after puberty has started. It has been shown that adolescent girls (but not boys) have insufficient calcium intake levels in the diet. The calcium deficiency occurs during a period of rapid bone growth, stunting the peak bone mass ultimately achieved; thus, these individual are at greater risk of developing osteoporosis.¹⁰ Milk and other dairy products are the most abundant source of calcium. In addition to calcium, protein plays a key role in bone mass acquisition. Besides adequate amount of vitamins C,D,K and minerals such as magnesium, zinc, are also important for bone health. Adolescents with average nutritional calcium intake bellow 1000 mg/day for boys and 850mg/day for girls will probably not reach optimal bone mass. The national osteoporosis foundation describes bone mass as analogous to a bank account in to which, during persons childhood, adolescents, and early adult hood, new bone ‘deposits’ are made to the skeleton faster than old bone is ‘withdrawn’. After the age 30, the rate of withdrawal exceeds the rate of deposit; therefore, establishing healthy bone mass in childhood and early adult hood is crucial.³⁰

Physical activity: girls and boys and young adults who exercise regularly generally achieve greater peak bone mass than those who do not. Physical activity is a determinant of peak bone mass^31. Sufficient exercise during childhood and adolescent, particularly the pre pubertal years, is more effective for increasing bone mass and strength than exercise in adulthood. ³²  Whether benefits achieved before puberty are sustained into adult hood remains to be determined by appropriate longitudinal studies. In healthy adults, vigorous exercise programs and resistance training of moderate to high intensity can preserve bone density^33. Weight bearing physical activity is important for maintenance of bone mass, and activities that increase muscles strength are also safe and beneficial, particularly for bones of the upper limb.³⁴ An optimal, exercise program should include activities for increasing strength, balance, flexibility and coordination of the upper and lower limbs and trunk. To influence BMD, physical activity undertaken 2-3 times per week and maintained for 20 to 60 minutes has been found to be helpful. Training intensity between 70 to 80 % of the functional capacity, or maximum strength can preserve bone density, but remain to be determined whether these are optimal for influencing BMD.³⁵ Low intensity exercise such as walking has minimal effect on BMD.³⁶ In adults, any skeletal benefit accrued from a exercise program will not be sustained, if an individual returns to a secondary life style.³²

 

Hormonal factor: sex hormone, including estrogen and testosterone, are essential for the development of bone mass. Beside growth hormone, thyroid hormone, PTH and calcitonin also play crucial roles. The pubertal growth spurt is related to the production of estrogen- the major female hormone. A certain content of body fat may be required to induce the onset of puberty. Adipose tissue mass is correlated tightly with whole body density in women but not in man. This fact brings into focus the notion that dietary indiscretions can have a profound effect on the overall process of fat production, menarche and estrogen protection. Women with eating disorders such as anorexia nervosa or bulimia have diminished body fat as well as abnormalities in menstrual function. These women develop insufficient bone mass either as a result of  loss of bone or as a result of deficient formation.^37,38

PATHOLOGICAL BASIS OF LOW BONE DENSITY

 

Definition of osteoporosis: The word osteoporosis is from the Greek osteon for “bone” & porous for “pore” or “passage”.  Indeed osteoporosis literally makes bone more porous. Osteoporosis is a generic term referring to a state of decreased mass per unit volume (density) of normally mineralized bone. Clinically, osteoporosis is synonymous with low bone density. In 1991, a panel of experts arrived at a consensus definition of osteoporosis as a systemic disease characterized by low bone mass and micro architectural  deterioration of the skeleton, leading to enhance bone fragility and increased fracture risk³⁹ This definition encompasses the two important skeletal changes in osteoporosis namely, diminished bone mass and diminished bone quality. However, this is not a practical definition for patient care, because the only means of assessing bone quality (other than fragility fracture) is histologic study of bone biopsy specimens.

The short comings of this definition led the World Health Organization (WHO) to convene a new panel of experts to define just what is meant by the term “low bone mass”⁴⁰. The group began its deliberations by agreeing on two basic concepts. First, they assumed that fracture risk must be lowest when BMD is highest – sometimes between ages 20 and 40 in healthy people. The relative risk for fracture in this reference group was arbitrarily set at 1.0. Second, the expert panel agreed, on the basis of several studies⁴¹ that relative risk for fracture double for each standard deviation (SD) decrement in BMD. Thus, in patient’s in whom BMD is 1SD below the mean for peak bone mass, the relative risk is 2.0. If the value is 2 SD below the mean, the risk double 4.0. The relationship between BMD and fracture risk is continuous, and there is no fracture threshold. With these concepts in mind, the WHO panel developed the following working definitions:-

v         Normal is defined as BMD less than or equal to 1.0 SD below the mean for peak bone mass.

v         Low bone mass (osteopenia) is defined as more than 1.0 but less than or equal to 2.5 SD below the mean.

v         Osteoporosis is defined as more than 2.5 SD below the mean.

These definitions were developed for epidemiologic studies but have been adapted as “Diagnostic Criteria” in much the same way that arbitrarily selected cut points are used to define hypercholesterolemia and hypertension.

 

Prevalence of osteoporosis:– Women of all races and ethnic origin are susceptible to osteoporosis and fracture. But whites, especially of northern European descent, and Asian are at increase risk for osteoporosis., Osteoporosis is not a just a disease of women, and there are compelling reasons for men to join the fight for better access to screening and more equitable reimbursements for screening. Two million of the total 10 million individuals diagnosed with osteoporosis in 1995 were male. Another 3 million men are at risk. Studies completed in 1994 showed that a 50 year old man has a remaining life time risk of osteoporotic fracture of 13% and experiencing such a fracture has more direct implication for man than women: while the rate of hip fracture is two to three times higher in women then men, the one year mortality following a hip fracture is nearly twice as high for men as for women. The statistics paint a chilling portrait of the future for men suffering from osteoporosis. Each year, men suffer 1/3 of all hip fracture that occurs, and 1/3 of these men will not survive more than a year. Over 100,000 men have a hip fracture every year, 1/3 of these men will die of complication from their hip fracture within a year. Of the survivors, more then a quarter will not walk again without assistance. In addition to hip fracture, men also experience painful and debilitating fracture of the spine, wrist, and other bones due to osteoporosis. In type 1 and type 2 osteoporosis, women are affected more than the men, with female to male ratio of 6:2 and 2:1 respectively. In secondary osteoporosis, both sexes are equally affected. The peak incidence of type 1 osteoporosis is in people aged 50 to 70 years, and peak incidence for type 2 is in people aged 70 years or older. Secondary osteoporosis can occur in persons of any age. Accordingly to US census bureau, international database, 2004, 1.45 crore people among 14.13 crore population of Bangladesh are suffering from osteoporosis, which is 10.26 percent of total population. 6.62% patient’s of osteoporosis are under diagnosed world wide and in Bangladesh 0.93 crore are undiagnosed which is 64.13 % of the total osteoporotic patient. Recent National Health and Nutrition Examination Survey (NHANES III, 1988-1994)⁴² review dual energy x-ray absorptiometry measurements of femoral BMD in a non-Hispanic white population. This snapshot determined peak bone mass in 382 men and 409 women 20 to 29 years of age. According to the WHO criteria, 13% to 18% of women aged 50 or older had osteoporosis, another 37 % to 50% had low bone mass. From the most recent US census data, this translates to 4 to 6 million women with osteoporosis and 13 to 17 million with low bone mass; in men over age 50, the corresponding members are 1 to 2 million with osteoporosis and 4 to 9 million with low bone mass.⁴³ The definition of low bone mass includes persons in whom risk of fracture is at least double that for healthy young adults. Therefore, about 22 million to 34 million Americans aged 50 are currently at increased risk for fracture.

Costs of care: Complication of osteoporosis are major community health problem in terms of both people and healthcare dollars. The estimated cost fractures complicating osteoporosis in 1995 was a staggering $13.8 billion.⁴⁴  Most of this money ($10.3 billion, or 75%) was spent for treatment of fracture in white women.⁴⁵ These investigation confirmed the well recognized observation that osteoporosis is principally a problem of ageing white women. Nonetheless, a full 23% of health care expenditures for this disease were incurred by white men (18%) and non-white women (5%). Even the group least susceptible to osteoporotic fracture, non-white men, required $200 million in osteoporosis care in 1995. Most money (63%) went for care of hip fracture, but 37% dollars were spent on other types of fractures. While every effort was made to capture relevant data, fractures other than hip fractures were probably under reported, because most of them do not require hospital admission⁴⁴.

Morbidity and mortality from hip fractures: Some studies have documented substantial in hospital mortality in patient’s with hip fracture; estimates range from 4% to 11.5%.⁴⁶ Other studies have shown that this mortality rate remains high for several years after a fracture. In one report, excess in death per 100 cases was 14 during the 5 years after fracture to patient’s who had little functional impairment or low co morbidities before fracture. The fact that the patient’s general health status is important in assessing the risk of mortality after hip fracture is obvious.⁴⁷

In one study, the 3month mortality was 13.5%, compared with 2.6% in a match Cohort. However, if the fracture occurred in an institution the 3 months mortality was 23%, compared with 10% for institutionalized patient’s who did not sustain a hip fracture. ⁴⁸

Serving a hip facture is not the end of the study. A Mayo clinic study of men who do had broken hips showed that more than half needed to be discharged to nursing homes. Among those who survived, 97% still resided in nursing homes or in for terminal care facilities or required home health care 1 year later. Only 41% of these men had recovered their pre fracture functional status after 1 year.⁴⁹ Given this high morbidity and mortality, a great deal of attention has been paid to factors that influence the out comes from hip fractures. The findings are predictable: out come are poorest for patient’s over age 85 years, these with coexisting functional problems, and those with scores of 3 or 4 on the American society of anesthesiologists rating of operative risk. For as yet in unexplained reasons, being male is predictor of unexplained hip fractures that carry a poor prognosis.

Most in hospital death (65%) result from cardiovascular events, and a history of congestive heart failure, angina, or chronic pulmonary obstructive disease contributes substantially to mortality. According to one study, postoperative aspirin administration reduced the risk of dying in hospital by 75%, an important observation that requires additional verification.

In another study of relatively healthily population sustaining hip fracture in their own homes and discharged to their homes, gait and balance were reviewed 2 months after fracture. A 17% increase in 2year mortality was shown for each unit decrease in the balance score (range, 0 to 17), but poor gait were not associated with an increased likelihood of readmission to hospital. However, both poor balance and poor gait ware associated with a substantially increased likelihood of nursing home admission.⁵⁰

Pathogenesis of osteoporosis:

Skeletal fragility can result from: (a) failure to produce a skeleton of optimal mass and strength during growth; (b) excessive bone resorption resulting in decreased bone mass and micro architectural deterioration of skeleton; (c) an inadequate formation response to increased resorption during bone remodeling. In addition, the incidence of fragility fractures, particularly of the hip and wrist, is further determined by the frequency and direction of falls.

To understand how excursive bone resorption and inadequate formation result in skeletal fragility, it is necessary to understand the process of bone remodeling, which is the major activity of bone cell in the adult skeleton. The bone remodeling or bone mullicellular unit (BMUs) described many years ago by Frost and others⁵¹ can occurs either on the surface of trabecular bone as irregular Howship lacunae or in cortical bone as relatively uniform cylindrical Haversian systems. The process begins with the activation of hematopoietic precursors to become osteoclasts, which normally requires an interacuion with cells of the osteoblastic lineage. Because the resorption and reversal phases of bone remodeling are short and the period required for osteoblastic replacement of the bone is long any increase in the rate of bone remodeling will result in a loss of bone mass. Moreover, the larger member of unfilled Howship lacunae and Haversian canals will further weaken the bone. Excessive resorption can also result in complete loss of trabecular structures, so that there is no template for bone formation. Thus, there are multiple ways in which an increase in osteoclastic resorption can result in skeletal fragility. However, high rate of resorption are not always associated with bone loss; for example, during the pubertal growth spurt. Hence an inadequate formation response during remodeling is an essential component of the pathogenesis of osteoporosis.

Central role of estrogen: The concept that estrogen deficiency is critical to the pathogenesis of osteoporosis was based initially on the fact that post menopausal women, whose estrogen level naturally decline, are at highest risk for developing the disease. Morphologic studies and measurement of certain biochemical markers have indicated that bone remodeling is accelerated at the menopause as both markers of resorption and formation increased.⁵² Hence, contrary to Albright’s original hypothesis, an increase in bone resorption, and not impaired bone formation, appears to be the driving force for bone loss in the setting of estrogen deficiency. But rapid and continuous bone loss that occurs for several years after the menopause must indicate an impaired bone formation response, since in younger individuals going through the pubertal growth spurt, even faster rates of bone resorption can be associated with an increase in bone mass. However, the increased bone formation that normally occurs in response to mechanical loading is diminished is estrogen deficiency, suggesting estrogen is both anticatabolic and anabolic.⁵³

Estrogen deficiency continues to play a role in bone loss in women in their 70 s and 80s, as evidenced by the fact that estrogen treatment rapidly reduces bone breakdown in these older women. More over, recent studies in humans have shown that the level of estrogen required to maintain relatively normal bone remodeling in older post menopausal women is lower than that required to stimulate classic target tissue such as the breast and uterus. Fracture risk is inversely related to estrogen level in post menopausal women, and as little as one-quarter of the dose of estrogen that stimulate the breast and uterus is sufficient to decrease bone resorption and increase bone mass in older women. This greater sensitivity of the skeleton may be age related.⁵⁴

Estrogen is critical for epiphyseal closure in puberty in both sexes and regulates bone turnover in men as well women. In fact, estrogen has a greater effect than androgen in inhibiting bone resorption in men; although androgen may still play a role.⁵⁵ Estrogen may also be important in the acquisition of peak bone mass in men. Moreover, osteoporosis in older men is more closely associated with low estrogen than with low androgen levels.⁵⁶

Estrogen deficiency increases and estrogen treatment decreases, the rate of bone remodeling, as well as the amount of bone lost with each remodeling cycle. Studies in animal models and in cell culture have suggested that this involves multiple sites of estrogen action, not only on the cells of the BMU but on other marrow cells. Estrogen acts through 2 receptors: Estrogen receptor  (ER) and ER . ER appears to the primary mediator of estrogen’s actions on the skeleton.⁵³ Osteoblast do express ER but actions of ER agonist on bone are less clear. Some study suggest that the effect of estrogen signaling through ER and ER are in opposition, while other study suggest that activation of this two receptors has similar effects on bone.⁵⁷

Single nucleotide polymorphisms (SNPs) of ER may affect bone fragility. In largest study to date, 1 of the SNPs for this receptor was associated with a significant reduction in fracture risk, independent of bone mineral density (BMD). Other studies have suggested that SNPs of ER can affect BMD and rates of bone loss as well as fracture risk in both men and women.⁵⁸

An orphan nuclear receptor, estrogen receptor related receptor  (ERR), with sequence homology to ER and ERR, is also present in bone cells.⁵⁹ Despite its inability to bind estrogens, this receptor may interact with ER and ER or act directly to alter bone cells function. A regularly variant of the gene encoding ERR was recently found to be associated with a significant difference between lumbar spine and femoral neck BMD in premenopausal women.⁶⁰

Sex hormone-binding globulin (SHBG), the major protein for sex steroids in plasma, may not only alter the bioavailability of estrogen to hormone-responsive tissues but also affect its entry in to cells. Epidemiologic studies suggest that SHBG may have a effect on bone loss and fracture risk independent of the effect as a binding protein.⁶¹

While estrogen can act on cells of the osteoblastic lineage, its effect on bone may also be dependent on actions on cell of the hemotopoietic lineage, including osteoclast precursors, mature osteoclasts and lymphocytes. Local cytokines and growth factors may mediate these effects. The effects of estrogen on cytokine production may be mediated by T cells.  A direct effect of estrogen in accelerating osteoclast apoptosis has been attributed to increased TGF- production.⁶²

Calcium, Vitamin D, and parathyroid hormone:

The concept that osteoporosis is due to primarily to calcium deficiency particularly in the elderly, was initially put forward as a counter proposal to Albright’s estrogen deficiency theory. Decreased calcium intake, impaired intestinal absorption of calcium, due to aging or disease, as well as vitamin D deficiency can result in secondary hyperparathyroidism.  The active hormonal form, 1, 25, dihydroxy vitamin D (calcitriol), is not only necessary for optimal intestinal absorption of calcium and phosphorus, but exerts atonic inhibitory effect on parathyroid hormone (PTH) synthesis, so that there are dual path ways that can lead to secondary hyperparathyroidism.⁶³ Vitamin D deficiency and secondary hyperparathyroidism can contribute not only to accelerated bone loss and increasing fragility, but also to neuromuscular impairment that can increase the risk of fall.⁶⁴ Clinical trial involving older individuals at high risk for calcium and vitamin D deficiency indicate that supplementation of both can reverse secondary hyperparathyroidism, decrease bone resorption, increase bone mass, decrease fracture rate, and even decrease the frequency of falling.⁶³ However, in a large recent study, calcium and vitamin D supplementation did not reduce fracture incidence significantly, perhaps because this population was less deficient in Vitamin D.⁶⁵

Polymorphisms of the VDR have been studied extensively, but the results have been variable. This may be in part because the effect of a given polymorphism in this receptor is dependent on an interaction with the environment, particularly with calcium.⁶⁶ VDR polymorphism are also associated with deficiency in the response to therapy with calcitriol.⁶⁷ There is also evidence for an effect on fracture risk independent on bone density and bone turnover, which might be due to an alteration in the frequency of falls.⁶⁸

Secondary hyperparathyroidism present when there is relative insufficiency of vitamin D, that is, where the level of circulating form-25- hydroxy vitamin D- fall below 30ng/ml, suggesting that the target for vitamin D supplementation should be at this level or higher.⁶⁹ The seasonal decrease in fractures, independent of the increase in rate of falls.⁷⁰ In addition, increase PTH level are associated with increased mortality in the frail elderly, independent of bone mass and vitamin D status. The precise mechanism underlying this relationship have not yet been determined, but the risk of cardiovascular death was increased.⁷¹ Polymorphism of the calcium sensing receptor, which regulates calcium secretion by suppression of PTH translation and PTH secretion, have not yet been associated with any alteration in bone phenotype.

Receptor activator of NF-, its ligand, and osteoprotegerin:

The concept that stimulation of bone resorption requires an interaction between cells of the osteoblastic and osteoclastic lineages was put forward many years ago, but its molecular mechanism was only identified recently.⁷² Three members of the TNF and TNF receptor super family are involved; Osteoblast produce RANKL, a ligand for receptor activation of NF-B (RANK) on haemopoietic cells, which activates the differentiation of osteoclasts and maintain their function. Osteoblasts also produce and secrete osteoprotegerin (OPG), a decoy receptor that can block RANKL/RANK interactions. Stimulators of bone resorption have been found to increase RANKL expression in osteoblasts, and some also decrease OPG expression.⁷³ Bone cell appear to express the membrane-bound form of RANKL, and thus, osteoblasts must physically interact with osteoclasts precursors in order to activate RANK. Soluble RANK can be produced by activated T lymphocytes and is as active as membrane-bound RANKL in binding to RANK.⁷⁴ Recently a monoclonal antibody against RANKL was shown to produce prolonged inhibition of bone resorption in post menopausal women.⁷⁵ It was also shown that RANKL level were increased on the surface of bone marrow cells for early post menopausal women who were estrogen deficient.⁷⁶ However, it has been difficult to demonstrate a role for OPG deficiency in the pathogenesis of osteoporosis. Since OPG levels are not consistently altered, OPG level increase with age, and it is possible that OPG production rises as a homeostatic response to limit the bone loss that occurs with an increase in other bone resorbing factors.⁷⁷ Polymorphism in the OPG gene have been associated with osteoporotic fracture and differences in BMD.⁷⁸ OPG Polymorphisms have also been linked to coronary artery disease.⁷⁹

The RANKL/RANK interaction is critical for both differentiation and maintenance of osteoclast activity and hence represents a final common pathway for any pathogenetic factor in osteoporosis that acts by increasing bone resorption, while it is assumed that cells of the stromal / osteoblastic lineage are the major source of RANKL in physiologic bone remodeling, other cells may act as a source of RANKL in pathologic states; for example, T cell production may play a role in osteoporosis as well as inflammatory bone loss. ⁸⁰

Recently a second system that might affect the interaction between osteoblast  and osteoclast has been identified.⁸¹ This involves the membrane adapter DNAX-activating protein 12 and Fc receptor common chain. Deletion of this molecule results in severe osteoporosis in mice. The molecules are involved in signaling through the immunorecptor tyrosine-based activation motif (ITAM). Co-operation between RANKL and ITAM signaling may be essential for osteoclastogenesis, for which nuclear factor of activated T cells (NFAT) is the master transcription factor.

 

Genes determining osteoblast differentiation and function:

Recent discoveries of signal transduction pathways and transcription factors critical for osteoblast differentiation and function have opened up new approaches to understanding the pathogenesis of osteoporosis. Gene deletion studies have shown that absence of runt-related transcription factor 2 (Runx2) or a downstream factor, osterix, are critical for osteoblast differentiation.⁸² Interestingly, over expression of Runx2 leads to a decrease in bone mass. ⁸³ A role for polymorphism of these transcription factors in osteoporosis had not yet been identified.

The recent identification of the critical role for the Wnt signaling pathway in regulating osteoblast function is of particular interest, since it has been shown to play an important role in determining bone mass and strength. LDL-receptor-related protein 5 (LRP5) interacts with the frizzled receptor to transduce signaling by Wnt ligands. A mutation of LRP5 that leads to constitutive activation can result in an increase in bone density.⁸⁴ The phenotype of families with LRP5 activating mutations varies considerably, although all show a striking absence of fractures. Some have normal skeletal structure, while others show abnormalities due to skeleton overgrowth.⁸⁵ Deletion of LRP5 results in a severe osteoporotic syndrome associate with abnormal eye development.⁸⁶ Polymorphism of LRP5 have been associated with differences in bone mass and fractures.⁸⁷ Mutation of LRP5 have been identified in a few patient’s with idiopathic juvenile osteoporosis.⁸⁸ However, Wnt signaling it also critical in bone development and can affect peak bone mass. ⁸⁹ The inhibition of skeletal growth by glucocorticoids may be mediated by effects Wnt signaling. The precise mechanism whereby Wnt signaling alters osteoblast function are not fully understood, but there is evidence that the canonical-catenin pathway is involved and that there is an interaction with bone morphogenetic protein 2 (BMP2).⁹⁰ There are a number of inhibitors that have been shown to interact with BMP2 and with the Wnt signaling pathway. One of these, Sclerostin, the product of the SOST Gene, has been shown to inhibit both BMP2 and Wnt signaling. Another potential inhibitory factor is the production of secreted frizzled-related protein (SFRP) by osteoblasts.⁹¹

Local and systemic growth factor:

Remodeling imbalance, characterized by an impaired bone formation response to increased activation of bone remodeling, is an essential component of the pathogenesis of osteoprosis.⁹² This may be due, in part, to an age-related decrease in the capacity of osteoblasts to replicate and differentiate. However, it seems likely that specific defects in the production or activity of local and systemic growth factor which also contribute to impaired bone formation BMPs as well as other members of the TNF family have been implicated. IGF, which is both a systemic and local regulator, as well TGF-, can also alter bone formation. There are some association between BMD and the incidence of the osteoporotic fracture and polymorphisms in the genes encoding IGF-1 and TGF-.⁹³ But the largest study to date, in Icelandic and Danish Cohorts, suggests that polymorphisms of the BMP2 gene are linked to low BMD and fracture risk.⁹⁴ Inhibition of local IGF-1 production may be an important component of glucocorticoid- induced osteoporosis as well as inhibition of growth in childhood.⁹⁵

Cytokines, prostaglandin’s, NO, and leukotrienes:

The concept that locally produced cytokines such as IL-1 and prostaglandin such as prostaglandin E₂ (PGE₂) can affect bone in more than 30 years old.⁹⁶ Subsequently, many cytokines were found to either stimulated or inhibits bone resorption and formation.⁹⁷ Prostaglandins have both stimulatory and inhibitory actions; however, the predominant effect of PGE₂, which is the major prostaglandin produced by bone cells, is to stimulate both resorption and formation.⁹⁸ The possibility that these factors might also be involved in the pathogenesis of osteoporosis is based largely on animals studies of bone loss after ovariectomy.⁹⁹ However, there is evidence that polymorphisms of IL-1, IL-6, TNF- and their receptors can influence bone mass in human.¹⁰⁰

Postaglandins, particularly PGE₂, are produced by bone cells largely through the action of inducible cyclooxygenase 2 (COX2). COX2 is induced by most of the factors that stimulates bone resorption and thus may enhance the response to these agents.⁹⁸ Treatment with COX-2 inhibitor blunt the response to impact loading and fluid shear stress, indicating that prostaglandins play an important role in the response of mechanical forces, and this may be enhanced by estrogen,¹⁰¹ In epidemiologic studies, small increases in BMD and decrease in fracture risk have been reported in individuals using NSAIDS, ¹⁰²

NO is produced by bone cells and is a cofactor for the anabolic response to mechanical loading.¹⁰³ However, unlike prostaglandins, NO may inhibit bone resorption, perhaps by increasing OPG production.¹⁰⁴ This effect may be responsible for the increase in BMD that has been demonstrated in patient’s treated with isosorbide mononitrate and other activators of the NO pahway.¹⁰⁵

Leukotrienes, the products of lipoxygenase, can affect bone by stimulating resorption and inhibiting formation.¹⁰⁶ Recently, arachidonate15-lipoxygenase, was identified as a negative regulator of bone density in mice,¹⁰⁷ and polymorphisms in the human gene, ALOX15, were found to be associated with differences in peak BMD in postmenopausal women. ¹⁰⁸

Collagen abnormalities:

A Polymorphism of the first intron of the gene coding for the type 1 collagen 1 chain and increased level of homocysteine can influence fracture risk independent of BMD.¹⁰⁹ This may be due to differences in helix formation or cross-linking of collagen, challenging the concept that mineral and matrix composition are normal in osteoporosis and that only structural abnormalities account for skeletal fragility.

Leptin and neural pathways:

Leptin deficiency or resistance is associated with high BMD in mice despite the fact that gonadal function is diminished.¹¹⁰ This has been attributed to a central effect on adrenergic signaling. Increased  adrenergic activity can decrease bone mass, but other neural pathways may be involved.¹¹¹ Some, but not all, epidemiologic studies suggest that -adrenergic blockers can decrease fracture risk and increase BMD.¹¹² Another neural pathway has recently been implicated by the finding that mice in which the canabinoid  type-1 receptor is activated, as well as mice treated with antagonist of this receptor, are protected from ovariectomy-induced bone loss.¹¹³

Risk factors for low BMD:      

Bone mass reflects the mass accumulated during growth, less any bone mass that has been lost since the adult peak was attained. A strong genetic component is apparent in peak bone mass. In addition, maximum bone mass is influenced by diet (calcium, protein) and exercise. Children with many disease or condition that interferes with growth, nutrition, and exercise have suboptimal bone mass. Recent studies suggest that use of long-acting contraceptives, such as medroxyprogesterone acetate, may limit skeletal growth during puberty, but this observation requires confirmation.¹¹⁴

In women, BMD is stable from the mid-20s to the earliest stages of the climacteric and then declines as estrogen production falls. In men, the timing and mechanism of normal bone loss are less well understood. Many circumstances shorten the time during which peak BMD is stable (table-1). Most of these are not influenced by changes in diet and life style alone, which is an important difference between osteoporosis and hypertension on hypercholesterolemia. Exceptions are cigarette smoking,¹¹⁵ and excessive use of alcohol, which have adverse effect on skeleton as well as on most other organ systems. Each of the circumstances listed in the table has an impact on the skeleton at any time in life. The effect is aggravated if coupled with lower estrogen level after menopause.

Table-1 Disease and conditions associated with low bone mass

Hormone excess

Parathyroid hormone, primary and secondary

Thyroxin, endogenous and exogenous

Cortisol, endogenous and exogenous

Hormone deficiency

Estrogen, premenopause (may be linked with anorexia, bulimia, athletic amenorrhoea, premature menopause, prolactinoma, hypopituitarism)

Estrogen, postmenopause

Testosterone, primary and secondary testicular failures.

Vitamin D metabolites, inadequate intake or malabsorption

Miscellaneous (not necessarily mediated by hormonal abnormalities)     

Medical conditions

v  Gastrectomy

v  Idiopathic hypercalciuria

v  Systemic mastocytosis

v  Prolonged immobilization (paraplegia, quadriplegia)

Lifestyle factors

v  Cigarette smoking

v  Excessive ingestion of caffeine

v  Excessive sodium intake (promotes hypercalciuria)

Medications

Heparin, warfarin, cyclosporine

One condition that requires special mention is idiopathic hypercalciuria in a patient with a calcium containing kidney stone. The ‘reflex’ response is to restrict dietary calcium intake so urinary calcium excretion declines and the risk of additional stone formation falls. This is not necessarily a good idea, since many such patient’s have a renal calcium leak that is not influenced by diet. This renal leak promotes a negative calcium balance, and the skeleton pays the price in an attempt to preserve balance. Eliminating calcium from diet exacerbates the negative calcium balance and further compromises the skeleton.

Corticosteroids are best known of the medications that decrease BMD. Long term experience with inhaled Corticosteroids does not yet confirm that they are less detrimental to the skeleton than other Corticosteroids, but initial studies suggest this might be the case.¹¹⁶

Thyroid disease also can cause problems with bone mass. Many women are receiving thyroid replacement therapy for hypothyroidism, which is appropriate if the disease is well documented and if replacement is not excessive (ie, serum thyrotropin level remains within the normal range and is not suppressed). Otherwise, chronic mild, symptomatic iatrogenic hyperthyroidism probably increases bone loss, and long-term overmedication with thyroxin result in low BMD.

 

Other risk factors for fracture:

A history of fracture, apparently even traumatic fractures before menopause but especially low-impact fractures after menopause, substantially increase the risk.¹¹⁷ A family history of fragility fractures (after trauma equal to or less than a fall from a standing height) is a significant contributory to fracture risk. Given the scant attention paid to osteoporosis until recently, this information is often missing from or incorrect in the patient history.

Body habitus is also an important factor in hip fracture risk with fractures being more than twice as likely in women 5ft 8in, or taller than women 5ft 2in, or shorter.¹¹⁸ the corresponding heights for men are 6ft and 5ft 9in.¹¹⁹

 

Women in the lowest quartile for body weight are also at increased risk for fracture, whilewomen who gained weight after age 25 are at lower risk of fracture.¹²⁰

Iatrogenic hip fractures probably occurs, and the risk increases with use of long acting benzodiazepins.¹²¹ On the positive side, reasonable evidence suggests that thiazide diureric therapy offers some protection against hip fractures in elderly patient’s.¹²² This does not imply that thiazides should be prescribed to treat osteoporosis or prevent hip fractures. However, if a diuretic is indicated is a patient at risk for fracture because of age and low bone density, thiazides should be considered.

The high incidence of vitamin deficiency, even in the well elderly in the United States, is receiving a great deal of attention.¹²³ A prospective, controlled study in France showed that daily supplementation with 100 mg of calcium and 800IU of vitamin D significantly decrease the incidence of hip fracture in a nursing home population. Whether this occurs through an effect on BMD or because of the known beneficial effects of vitamin D on striated muscle was not established. This investigation did demonstrate that the supplements corrected mild hyperparathyroidism. ¹²⁴

Other studies have shown that a high rate of bone turnover may be associated with an increased hip fracture risk independent of BMD. The effects of high bone turnover and low BMD were additive in terms of risk fracture. Thus, it would seem cost effective to provide 1,000 mg of calcium and 800 IU of vitamin D daily to everyone in the United States age 75 or older.^{125, 126}

Many simple, objective measures of frailty can help assess the risk of hip fracture. These include ability to rise from a chair without use of the arm, depth perception, contrast sensitivity, and gait and balance assessment. Simply put, any condition that increase the risk of falling in the elderly increase the risk of fracture.¹²⁷

Types of osteoporosis: 

Osteoporosis may be either a primary or a secondary form. Primary osteoporosis is the more common form and due to the typical age related loss of bone from skeleton. Primary osteoporosis is classified as type-1 and type-2. Secondary osteoporosis results from the presence of other disease or conditions that predispose to bone loss and is classified as type-3.

Type-1: Type-1 or postmenopausal osteoporosis occurs in 5% to 20% women, affecting those within 15 to 20 years of menopause,¹²⁸ with a peak incidence in the 60s and early 70s. The incidence in women is eight times higher than that in men.¹²⁹ The frequency of postmenopausal osteoporosis accounts for the overall female-male ratio of 2 : 1 to 3 : 1.

Estrogen deficiency is thought to underlie this from of osteoporosis, rendering skeleton more sensitive to parathyroid hormone (PTH) resulting in increased calcium resorption from bone. This in turn decreases PTH secretion, 1-25 -dihydroxy-vitamin D production, and calcium absorption and ultimately causes loss of trabecular bone, leading to vertebral crush fracture and colles’ fracture.

Women can loss around 2% to 3% of their bone per year for the first 5 years after menopause. Because of the low estrogen production, women loss nearly 50% of their trabecular bone and 35% of their cortical bone through their life time, whereas men loss only 25% of both types of bone. At least 75% of bone loss that occurs in women during the first two decades after menopause can be attributed to lack of estrogen rather than aging. Bone loss associated with menopause dose not begins with the onset of amenorrhoea but may occur 1 to 3 years before the actual cessation of menstrual periods.¹³⁰

Type-2: Type-2 osteoporosis or senile osteoporosis occurs in women or men more than 70 years of age and usually is associated with decreased bone formation along with decreased ability of the kidney to produce1,25,(OH)₂D₃. The vitamin D deficiency results in decreased calcium absorption, which increases parathyroid hormone (PTH) level and therefore, bones resorption. In type-2 osteoporosis, cortical and trabecular bone is lost, particularly leading to increased risk of hips, long bones, and vertebral fractures.

Type-3: Type-3 or secondary osteoporosis occurs equally in men and women and at any age. In men, most cases are due to disease or to drug therapy, but in 30% to 45% of affected individuals no cause can be identified.¹³¹ In various series of osteoporotic patient’s, secondary osteoporosis accounts for about 40% of the total number of osteoporotic fracture seen by a physician.¹³²

This type of osteoporosis is associated with variety of conditions, including hormonal imbalance (eg. Cushing’s syndrome); cancer (notably multiple myeloma); gastrointestinal disorders (especially inflammatory bowel disease causing malabsorption); drug use (eg. corticosteroid, cancer chemotherapy, anticonvulsants, heparin, barbiturates, valproic acid, gonadotrophin-releasing hormone (GnRH), excessive use of aluminum containing antacids); chronic renal failure; hypothyroidism, hypogonadims in men; immobilization; osteogenesis imperfecta and related disorder; inflammatory arthritis (particularly Rheumatoid arthritis); and poor nutrition (including malnutrition due to eating disorders).^{133, 134, 135}

CLINICAL PRESENTATION OF LOW BONE DENSITY

 

Symptoms:

Osteoporosis is a clinically silent but progressive disease until fracture occurs. Since low bone density alone dose not cause symptoms, many patient’s with quite advanced osteoporosis remain asymptomatic until a fracture occurs. These fractures typically affect the forearm (Colles’ fracture), spine (vertebral fracture) and femur (hip fracture). Colles’ fracture and vertebral fracture most often occurs in women age 55 and above, where as hip fracture affect older individuals (aged 70+). Osteoporotic limb fractures are usually precipitated by falls, where as the precipitating factor in vertebral fracture is often being lifted or lifting a heavy weight. The clinical presentation of vertebral fracture is highly variable. Common clinical presentation include; increasing dorsal kyphosis (Dowager’s hump), loss of weight and back pain. Skeletal back pain may also be a symptom. Radiograph may show osteopenia. This finding indicates that at least 30% of bone mass has been lost.

Assessment:

The assessment of osteoporosis should include a through medical history to identify risk factor for low bone density and fracture, routine laboratory test to rule out secondary causes, a physical examination to identify signs and symptoms of fractures, and bone mineral density (BMD) testing.

History and physical examination:

The history and physical examination are neither sensitive enough nor sufficient for diagnosing primary osteoporosis. However, they are important in screening for secondary forms of osteoporosis and directing the evaluation. A medical history provides valuable clues to the presence of chronic conditions, behaviors, physical fitness, and the long term use of medications that could influence bone density.

Those already affected by complications of osteoporosis may complain of upper or mid thoracic back pain associated with activity, aggravated by long periods of sitting or standing, and easily relived by rest in the recumbent positions. The history should also assess the likelihood of fracture. Low bone density, a propensity to fall, grater height and prior fracture are indications of increased fracture risk.

The physical examination should be through for the same reasons. For example, lid lag, and enlargement or nodularity of the thyroid suggests hyperthyroidism. Moon faces, thin skin and buffalo hump suggest Cushing’s syndrome. Cachexia mandates screening for an eating disorder or malignancy. A pelvic examination is necessary for the complete evaluation of women. Osteoporotic fractures are a late physical manifestation. Common fracture sites are vertebrae, forearm, femoral neck, and proximal humerus. The presence of a Dowager’s hump (Spinal curvature) in elderly patient’s indicates multiple vertebral fractures and decreased bone volume.

Complications:

Vertebral fracture, a well recognized complication of osteoporosis, is the most common osteoporotic fracture. Less than one third of these fractures are clinically identified. Regardless of whether they are symptomatic or identified on imazing, vertebral fractures are associated with increased mortality and morbidity rates. Complications include back pain and decreased mobility, with consequent days of bed rest. Compression fracture of the vertebrae varies in degree from mild wedges to complete compression.

Disfiguring kyphosis (Dowager’s hump) is usually related to multiple wedge fracture of the dorsal vertebrae. Abdominal protrusion, which occurs as consequences of the kyphosis is an unrecognized aspect of osteoporosis. Height loss occurring as a consequence of vertebral fractures is one of the most distressing aspects of osteoporosis in many women.

Decreased pulmonary capacity is a known complication of kyphosis; if severe, this may lead to shortness of breath and pulmonary symptoms of restrictive lung disease. Also, the incidence of esophagitis is increased in patient’s with kyposis because of changes in the abdominal cavity. Once vertebral fracture occurs, the process may be relentless with ongoing further vertebral fractures and height loss despite correction of BMD. ^{136, 137}

 

 

Differential Diagnosis:

Endocrinologic diseases

Endocrinologic deceases include the following.

• Hypogonadism in men and women.
• Cushing’s syndrome
• Corticosteroid –induced osteoporosis
• Hyperthyroidism.
• Severe primary hyperparathyroidism

In patient’s with acromegaly, the effects of growth hormone excess on bone mass are controversial. Some studies show increase bone mass, and some studies show reduced bone mass. The latter findings may reflect accompanying hypogonadism, a frequent finding in acromegaly. However the data about bone mass and fracture in diabetes, acromegaly and endometriosis are conflicting.

A rare form of osteoporosis occurs during pregnancy or shortly after delivery. The presentation usually includes severe back pain and multiple vertebral fractures. About 70% of cases occur in first pregnancies, and recurrences are unusual. Most cases resolve spontaneously, and bone mass increases after the termination of breastfeeding. In many women, bone mass normalizes after 3 years. Only a small number of patient’s are disabled for months or years. Patient’s with osteoporosis of pregnancy are at increased risk for postmenopausal osteoporosis.

Osteoporosis occurring late in pregnancy may be related to poor diet or calcium and vitamin D deficiency, where as cases occurring during lactation seem to be related to excessive secretion of PTH-related peptide, which is responsible for calcium transport in the breast and for the mobilization of calcium from bone to milk.

 

Nutritional Deficiencies:

Nutritional deficiencies affect the skeleton by impairing the supply of calcium and vitamin D, leading to secondary hyperparathyroidism and osteomalacia. Such deficiencies can occur after gastric resection and in patient’s with short- bowel syndrome. In those with anorexia nervosa, nutritional deficiency is exacerbated by amenorrhea.

Immobilization:

Immobilization, either temporary or from permanent neurological deficit may cause bone loss from disuse.

Medication use:

Long term corticosteroid use constitutes the most common form of secondary osteoporosis in both men and women. Corticosteroids cause impaired osteoblast function and changes in calcium homeostasis, which lead to accelerated bone loss and fracture. In patient’s treated with prednisolone doses exceeding 7.5mg/d for more than 6 months, the prevalence of vertebral fracture 30-50%.

Agonist of gonadotropin-releasing hormone reduces circulating estrogen levels and thereby causes excessive bone loss. In premenopausal women, tamoxifen and Raloxifene interfere with the binding of estradiol to nuclear receptors and thereby impair the cellular action of the hormone.

In vitro experiments have shown that heparin reduces osteoblastic activity and decreases osteoblast adhesion to matrix proteins. Long-term treatment with heparin is a known cause of osteoporosis.

Both aluminum and lithium interfere with intracellular signaling, and aluminum also impairs osteoblast function and causes osteomalasia. Antiepileptic drugs, especially phenytoin, have been shown to interfere with vitamin D metabolism and to increase the risk of osteoporotic fractures.

 

Juvenile osteoporosis:

This type of osteoporosis affects children and is therefore unlikely to be confused with involutional osteoporosis. Juvenile osteoporosis is characterized by the occurrence of primarily vertebral and metaphysial fractures that lead to back pain and difficulty in walking. In most publications, boys are predominantly affected, but most children recover fully.

The National Institutes of Health (NIH) consensus Development Panel on Osteoporosis prevention, Diagnosis, and Therapy asserts that secondary causes of bone loss are more common in men and perimenopausal women than in postmenopausal women. According to the panel’s estimates, secondary cause are responsible for 30% to 60% of osteoporosis in men (mostly due to hypogonadism, glucocorticioid use, and alcoholism) and more than 50% of osteoporosis in perimenopausal women (mostly due to hypoestrogenemia, glucocorticoid use, excessive levels of thyroid hormone, and anticonvulsant use).¹³⁸

Laboratory Test:

Basic chemical analysis of serum is indicated when the history suggests other clinical conditions influencing the bone density. The tests presented in tables2¹³⁹ and 3¹⁴⁰ are appropriate for excluding secondary causes of osteoporosis.¹³⁹ These tests provide specific clues to serious illness that may otherwise have gone undetected and which, if treated, could result in resolution or modification of bone loss. Specific biochemical markers (human osteocalcin, bone alkaline phosphatase, immunoassays for pyrinoline cross-links and type 1 collagen-related peptides in urine) that reflect the overall rate of bone formation and bone resorption are now available. These markers are primarily of research interest and are not recommended as part of the basic workup for osteoporosis. They have a high degree of biologic variability and diurnal variation and do not differentiate causes of altered bone metabolism.^141-143

For example, measures of bone turnover increase and remain elevated after menopause but do not necessarily provide information that can direct management.

Table-2

Evaluation of secondary osteoporosis

Abnormal study result	Suggested pathology
Increased creatinine level	Renal disease
Increased hepatic transaminase level	Hepatic disease
Increased calcium level	Primary hyperparathyroidism or malignancy
Decreased calcium level	Malabsorption, vitamin D deficiency
Decreased phosphorus level	Osteomalacia
Increased alkaline phosphatase level	Liver disease, Paget’s disease, fracture, other bone pathology.
Decreased albumin level	Malnutrition
Decreased TSH level	Hyperthyroidism
Increased ESR	Myeloma
Anemia	Myeloma
Decreased 24 hour calcium excretion level	Malabsorption, vitamin D deficiency
TSH= Thyroid stimulating hormone; ESR= erythrocyte sedimentation rate.

Table-3

Direct laboratory assessment for secondary osteoporosis

Cause	Finding/test
Hypogonadism	Decreased testosterone level in men Decreased estrogen level in women Increased gonadotropin level (LH and FSH)
Hyperthyroidism	Decreased TSH level Increased T4 level
Hyperparathyroidism	Increased parathyroid hormone level. Increased serum calcium level. Increased 1, 25, hydroxyvitamin D level
Vitamin D deficiency	Decreased 25- hydroxy calciferol level
Hemochromatosis	Increased serum iron level Increased ferritin level.
Cushing’s syndrome	24 hours urine free cotisol excretion Over night dexamethason suppression test
Multiple myeloma	Serum protein electrophoressis-M spike and Bence Jones proteinuria Increased ESR Anemia Hypercalcemia Decreased parathyroid hormone
LH=luteinizing hormone; FSH= Follicule- stimulating hormone; TSH= thyroid- stimulating hormone; T4= thyroxin; ESR= erythrocyte sedimentation rate.

Methods for BMD measurement:

BMD is determined by measuring the amount bone mineral (calcium hydroxyapatite) per unit volume of bone tissue. X-rays or gamma rays are offen use to quantify BMD. In quantitative terms, BMD is the amount of calcium hydroxyapatite, or Ca10 (PO₄)6(OH) 2, perunit volume of bone tissue examined.

Common methods conventional radiography, quantitative CT (QCT), single- photon absorptiometry (SPA), dual-photon absorptiometry  (DPA), quantitative ultrasonography (QUS), and dual-energy X-ray absorptiometry (DEXA).

Bone density measurements can be performed by using X-ray methods, such as DEXA, QCT, and ultrasonic methods. The most accurate way to diagnosis osteoporosis is by measuring bone mass. DEXA scans can be used to detect small changes in bone mass by comparing the patient’s bone density to that of healthy adults (T score) and to age-matched adults (Z score).

A number of methods have been developed for the in vivo determination of bone density in patients at risk of osteoporosis. Two of the most frequently used methods are based on measuring the attenuation of a beam of electromagnetic radiation or ultrasound when it passes through the bone. Ultrasonic measurement of velocity through the bone has also been used to determine bone density.

Currently, DEXA is the most accurate and recommended method for BMD measurement. It is a sensitive technique and can detect changes in bone density only 6-12 months after a previous measurement is obtained. Density measurements of the spine or hip are used. The procedure takes approximately 20-30minutes. The radiation exposure is low at approximately 2.5 mrem.

Bone biopsy may be useful in unusual forms of osteoporosis, such as osteoporosis in young adults. Biopsy provides information about the rate of bone turnover and the presence of secondary form of osteoporosis, such as myeloma and systemic mastocytosis. Patient’s with high turnover usually respond better to antiresorptive drugs than other treatments. Bone turnover can also be evaluated by estimating certain biochemical markers, such as osteocalcin and deoxypyridinoline.¹⁴⁴

X-ray (plain x- ray):-

Conventional radiographs are relatively insensitive for demonstrating osteoporosis. At least 30% of the bone mass must be lost before it is recognized. At this stage, the radiographic changes of generalized osteoporosis are more prominent in the axial skeleton than elsewhere.

In the spine, the accentuated primary trabecular pattern produces a vertically striated appearance in the vertebral bodies. Likewise, the loss of trabecular mass causes accentuation of the cortical outline, which is described as picture framing of the vertebral bodies. The vertebral bodies may develop a biconcave shape or compression fractures. In trabecular bones, the loss of   trabecular bone may cause the metaphyses to appear radiolucent. Pathologic fractures may occur at multiple sites.

In trabecular bones, bone resorption may be distinguished in 3 sites: endosteal   envelope, intracortical (Haversian) envelope, and periosteal envelope. These changes are best depicted with magnification radiography and quantitated with radiogrametry.

Other radiographic manifestation of osteoporosis includes the following:

–          Involvement of the lower dorsal and lumber spine, proximal humerus, femoral neck, and ribs (These sites are most commonly affected).

–          Increased radiolucency of bones

–          Decreased number and increased thickness of trabeculae

–          Cortical thinning

–          Juxtra- articular osteopenia with trabecular prominence

–          Bone bars (reinforcement lines)

–          Insufficiency fractures

–          Vertebral wedge fractures, fish vertebrae, decreased heights of vertebrae and accentuation of the cortical outlines (also called picture framing)

The assessment of a reduced radiological shadow density varies from physician to physician. So, the sensitivity and reliability of standard radiography to assess BMD are poor and as a result, this technique can not be used to diagnose osteoporosis. Radiography of the thoracic and lumbar spine is indicated only to identify and confirm the presence of fracture or to exclude possible metastasis.¹⁴⁵

QCT Scan (Quantitative Computerized tomography):

QCT is generally used to measure bone density in the lumbar spine, though it can be applied to other parts of the skeleton, such as the forearm. The accuracy and scanning time depends on the type of CT scanner used. This technique is the only BMD-measurement method to provide a true volumetric measurement of bone density (in milligrams/cubic centimeters) and a separate measurement of trabecular and cortical bone density.

QCT has been used to assess vertebral fracture risk. It has been found to be superior to other methods for assessing age-related bone loss, for distinguishing fractures, and for diagnostic classification.

Recent development in the CT technology allows 3-dimensional (3D) Volumetric BMD analysis of the proximal femur and high-resolution CT (HRCT) allows the analysis for trabecular structure. QCT bone density measurement of the lumber spine can be performed on standard CT scanners with provision of specialized software, and peripheral QCT measurement can be obtained on specially designed small-bore CT scanners.

The measurements are accurate and precise and require a comparatively low radiation dose in comparison with that needed for a standard diagnostic CT procedure. QCT is more accurate than DEXA in measuring BMD, especially in the spine in the older population group, as CT avoids the effect of degenerative disease and extraneous calcification. Resent development in 3D QCT allows assessment of the hip and complicated situation in the spine, as when both scoliosis and vertebral fracture are present.

False positives/negatives: One major disadvantage of QCT is that artifacts hamper the CT data, reducing its accuracy. The usual sources of error include beam hardening, detected scatter, and system drift. The accuracy of QCT reading can be improved with careful attention to detail. Patient’s should be well centered and scanned by using consistent settings. Another limitation of QCT is a significantly higher radiation dose than that of DEXA.

The presence of excess fat in the marrow in trabecular bone in aging population introduces an error in the BMD measurement of 7-15% per 10% of fat. This problem can be resolved by using dual energy, but at the expense of double the radiation exposure to the patient. The accuracy error and precision of QCT are 5-8%.^{146, 147}

SPA (Single photon absorptiometry) Study: –

SPA was established in 1963 for the bone densitometric evalution of the appendicular skeleton. SPA uses a single-energy source of gamma rays (iodine 125; photon energy, 27.3 keV) or Am-241 (60keV) to produce a collimated pencil beam, which is tracked across the measurement site. The half-life of 125I is approximately 60 days, resulting in a useful life of around 6 months. The transmitted photons are counted by using a sodium iodide crystal/photomultiplier for each point along the track.

Because of the low photon flux and energy source, the technique is usually applied to a peripheral skeletal site, such as the forearm and, less commonly, the heel. The forearm chosen is the nondependent arm. To allow correction for soft tissue, the forearm must be placed in a water bath. The mean photon count through the water bath without the interposed limb is used as baseline value. A reduction in the photon count below this baseline is assumed to be due to the bone. Muscles of the forearm have attenuation effect similar to that of water. The effects of varying muscle mass are thus eliminated by the water bath.

Degree of confidence:

Although SPA was widely used and although provide valuable a research data, the radionuclide source is a disadvantage. The energy source is subject to decay and must be replaced regularly. The low photon flux can cause the scanning time to be long (up to 40min), and spatial resolution tends to be poor. SPA machines repeatedly scanned in a single line and were limited (because of the physics of their operating principle) to measuring bone sites that could be either immersed in water or embedded in material with adsorption properties equivalent to soft tissue (to stimulate homogenous overlying soft tissue)

False positives / Negatives:

The precision error (coefficient of variation) is 1% for SPA. The precision error is affected not only by the measurement of technique but also subject characteristics. Precision error tends to increase in an elderly or osteoporotic population due to factors such as greater difficulty in repositioning and lower mean BMD.¹⁴⁸

 

DPA (Dual Photon Absorptiometry) study               

DPA is an extension of the SPA principle that was developed to compensate for errors in SPA bone-mass measurement due to varying composition and thickness of surrounding soft tissues. This deficiency of SPA was over come by using 2 distinct photon energies, usually gadolinium¹⁵³. Photons of different energy are differentially attenuated by bone and soft tissue. Therefore, their absorption by bone, and hence bone density, can be calculated by measuring the percentage of each transmitted beam and then by applying simple simultaneous equations. The source of photons is 153Ga, which emits photons of 2 discrete energies (44 and 100 keV). The scanning approach is similar to that of SPA.

 

Degree of confidence:

DPA represents an improvement over SPA in that it allows the direct measurement vertebral or femoral bone density. DPA eliminates the need for a constant soft tissue thickness across the scanning path (allowing its use in areas such as the spine and femur). DPA can be used to quantify changes in patient’s with metabolic bone disease or in those undergoing treatment with drugs that alter bone mineral content.

The desirable characteristics of DPA include its capability in assessing vertebral, proximal femoral or total body bone content; its independence from effect of marrow fat and other soft tissue, and its relatively low radiation dose. However, it is more expensive than other techniques, it has a lower scanning time, and it is not as widely available as SPA.

False Positive/ Negative:

With DPA, the error of precision and accuracy is 2-3%. One unavoidable source of error in the dual-photon technique is the fat distribution in the path of the radiation beam. It is possible to correct for an evenly distributed fat layer across the scanning path, but an uneven distribution introduces error in to the measurements.¹⁴⁹

Ultrasound Measurement of Bone Density:                   

Finding: In 1984, Langton first described the measurement of broadband ultrasound attenuation (BUA) in the calcaneous as a potential indicator of hip fracture risk. The concept is based on the knowledge that the speed of sound and attenuation of sound wave are affected by density, compressibility, viscosity, elasticity, and structure of the material it is traveling though. This technique marked a departure from the conventional methods of bone density that used ionizing radiation. Ionizing radiation is attenuated at atomic level, whereas ultrasound is attenuated at the macroscopic structural level.  Some therefore, suggest that broadband ultrasound attenuation (BUA) depend on the macroscopic structure of cancellous bone in addition to the BMD assessed by using the ionizing radiation techniques.

BUA measurement in the calcaneus requires 1 transducer with 2 broadband ultrasound transducer components: one acts as a transmitter, and other acts as receiver. For a given material, ultrasound attenuation in always the same; this is known as the BUA index. To determine the attenuation index of any material (including bone) a broadband ultrasound frequencies is passed through the full thickness of material. The amplitude spectrums of the received signal in then compared with the spectrum of a reference material (water). By recording the frequency spectrum through water with and without the heel in position, a plot of attenuation with frequency is achieved. The difference between the 2 spectra is then plotted against frequency, giving a straight-line graph, the slope of which is the BUA index (in decibels per megahertz). The ultrasound frequencies used in the range of 0.1-1MHz. This range has become known as BUA.

Degree of confidence: QUS for bone analysis is a non-ionizing method in which the calcaneus as the measurement site. This technique is both a cost effective and accurate for identifying patients at risk of osteoporotic fracture. QUS has been scientifically validated in both fundamental in vitro studies and clinical in vivo studies. Clinical studies have shown that QUS parameters are sensitive to age related changes; they may be useful in distinguishing osteoporotic subject, and they offer a prospective prediction of fracture risk comparable to that of axial DEXA.

False positives/ Negatives: A number of factors can affect the accuracy and precision of BUA and produce false-positive or false-negative results. The anatomically incorrect placement of the region to be examined is 1 of these factors. Other factors are patient’s specific and may affect bone measurements; these are variability in bone width and soft tissue thickness or composition, marrow composition, and temperature. Error in measurement can be introduced by diffraction, which affect both attenuation and velocity measurements and is device specific.

 

DEXA (Dual Energy X-ray Absorptiometry):

DEXA is the method of choice to measure bone mineral density in elderly patient’s and others at risk of osteoporosis. Early detection is an important because fractures represent an enormous health burden. Central bone mineral density (BMD) measurement using DEXA is currently the gold standard for the diagnosis of osteoporosis.¹⁵⁰ DEXA measurement can be completed by in about 15 to 20 minutes with minimal radiation exposure (about one tenth that of a standard chest X-ray).

Peripheral DEXA scans are inexpensive and are useful in screening large populations such as at health fair. The peripheral DEXA device is simple to operate. However, the sensitivity of peripheral DEXA for detecting osteoporosis is lower than that of central DEXA. Moreover, issues such as a lack of consensus on how results from peripheral sites are interpreted, poor correlation among the different machines, and precision errors prohibiting monitoring the patient’s who are receiving osteoporosis therapy limit the clinical utility of this technology.

Indication for obtaining a DEXA scan

Menopausal women should be evaluated clinically for osteoporosis risk in order to determine the need for BMD testing. All woman aged 65 or older, younger postmenopausal women with risk factors, and men aged 70 or older should undergo bone density testing. Risk factors include dementia, poor health, recent falls, prolonged immobilization, smoking, alcohol abuse, low body weight (<127 lb), history of fragility fracture in a first degree relative, estrogen deficiency at an early age (<45 years), and steroid use for more than 3 months.¹⁵¹

Adult who have a history of fragility fractures, have diseases associated with bone loss, or take medication that causes bone loss should also have DEXA scans.¹⁵² DEXA scans are also appropriate for monitoring a patient’s response to osteoporosis therapy.¹⁵¹

Site of measurement of BMD

The International Society for Clinical Densitometry recommends obtaining BMD measurements of the posteroanterior spine and hip. The lateral spine and ward’s triangle region of the hip should not be used for diagnosis, because these sites overestimate osteoporosis and results can be false positive. T-scores represent the standard deviations (SDs) comparing a patient’s BMD to that of a young adult (control), whereas Z-scores compare a patient’s, BMD to that of age matched controls. The World Health Organization (WHO) defines osteoporosis as T-score of 2.5 or below is either the spine or the hip.⁴⁰

In the spine, the BMD of L₁ through L₄ should be reported unless there are vertebrae affected by severe degenerative changes or compression fractures. These should be excluded from the analysis because they falsely increased BMD. Most DEXA devices measure and report BMD of the total hip, femoral neck, and trochanter. The diagnostic classification of a patient is based on the lowest T-score of any of these hip sites.

Evidence suggest that the femur is the optimum site for predicting the risk of hip fracture¹⁵³ and the spine is the optimum site for monitoring response to treatment.¹⁵⁴ In very obese patient’s, those with primary hyperparathyroidism, or those in whom the hip or the spine, or both, can not be measured or interpreted, BMD may be measured in the forearm, using a 33% radius on the nondominant forearm.¹⁵¹

Interpretation of DEXA scans:   

Primary care physicians are usually not directly involved in the performance and interpretation of DEXA scans but should be familiar with the information on DEXA scan reports and how it applies to patient’s management.¹⁵⁵ T-scores are used to diagnose osteoporosis, and Z-scores give the physician a sense of the age-appropriateness of bone loss. A Z-score of 2.0 or lower suggests a secondary cause and should trigger the search for underlying causes.¹⁵⁶ In our practice, patient’s with a Z-scores below 1.0 are frequently found to have secondary causes, and such a score initiates a comprehensive search for these causes.

Although, postmenopausal osteoporosis is clearly the most common bone disease, secondary causes of osteoporosis are also quite common. Physicians need to actively look for these causes, either by thorough history taking or with biochemical studies.

Initiation of treatment:

Evidence showing an unacceptably high risk of fracture with T-scores of 2.5 and below and a significant reduction in fracture risk with treatment has made this threshold the initial criterion for the diagnosis of osteoporosis.^155,156 However, the National Osteoporosis Foundation recommends initiating treatment to reduce fracture risk in women with T-scores below 2.0, even in the absence of risk factors, and in women with T-scores below 1.5 in the presence of one or more risk factors.¹⁵⁷ Regardless of the T-score, patient’s with previous vertebral or hip fracture are classified as severely osteoporotic and should be treated. Recently the National Osteoporosis Risk Assessment study found osteoporotic fractures among patient’s who were classified as oeteopenic on the basis of the WHO criteria. There is now a move toward establishing a global fracture risk score that includes risk factors and BMD as a possible basis for initiating therapy.¹⁵⁸

Monitoring response to treatment:

DEXA scans are useful in determining response to osteoporosis therapy. Under ideal conditions, the same technologist should perform DEXA scans on the same densitometer and under similar circumstances.

It is important to note that antiresorptive drug therapy leads to significant reduction of fracture risk, which can be obtained with very little improvement in BMD. Moreover, in interpreting serial DEXA scans, the actual BMD (in gm/cm²) should be compared and not the T-scores.

BMD remain the best and most useful marker for fracture risk reduction in clinical practice. The interval between BMD testing should be determined according to each patient’s clinical status. BMD measurements to monitor response to osteoporosis therapy should generally be obtained every year until stability is established, then at longer intervals, such as every 2 years.¹⁵¹ The posteroanterior lumbar spine is the optimum site to monitor therapy, and significant changes may be seen in a year or more, depending on the therapy used.¹⁵⁴ Medicare permits physicians to repeat DEXA scans every 2 years¹⁵⁷ or, in patient’s who are being monitored while on therapy, every year.

Osteoporosis in men:

The focus of osteoporosis management has been on postmenopausal women. However, osteoporosis in men is not rare.¹⁵⁹ The estimated lifetime risk of fracture ranges from 13% to 25%.¹⁶⁰ The three major causes of osteoporosis in men are alcohol abuse, glucocorticoid excess (from either endogenous Cushing’s syndrome or long-term glucocorticoid therapy), and hypogonadism.^160,161 Bone density testing should be considered in men with fragility fractures; those taking drugs that may cause bone loss, such as androgen deprivation therapy for prostate cancer¹⁶²; and men with multiple risk factors.

The International Society for Clinical Densitometry recommends that in men aged 65 years or older, osteoporosis should be diagnosed if T-scores are at or below 2.5. Between age 50 and 65years, osteoporosis should diagnosed if T-score are at or below 2.5 and other risk factors for facture are identified. In men under the age 50 years, diagnosis of osteoporosis should not be made on the basis of T-scores. Osteoporosis may be diagnosed clinically in men at any age with secondary causes of low BMD supported by the finding of low BMD.

It is important to know that the WHO classification, with its associated implications for fracture risk, was derived from a database composed purely of postmenopausal white women. Most densitometry devices now use the third National Health and Nutrition Examination Survey (NHANES III) database, which provide appropriate sex-matched controls for hip BMD.

Artifacts:

Certain conditions can artificially elevate the BMD, obscuring osteoporosis and leading to underestimation of fracture risk.¹⁶³ These include degenerative changes seen in osteoarthritis and ankylosing spondylitis, structural abnormalities such as compression fracture¹⁶⁴ and scolosis,¹⁶⁵ aortic calcification, high-density objects on clothing, surgical implants,¹⁶⁴ laminectomy,¹⁶⁵ and retained radiopaque contrast agents.¹⁶⁴ Vertebrae  with abnormal conditions should be excluded from the spine analysis. Similarly, BMD at the proximal femur can be altered by degenerative arthritis, degree of internal rotation, placement of soft tissue gluteal silicon implants,¹⁶⁶ and overlying soft tissue thickness or fat.¹⁶⁷ Patient’s positioning and appropriate placement of region of interest are paramount for precision and reproducibility.¹⁶⁵ Physician should visually assess DEXA scans for artifacts that could affect BMD values. Going down the spine, the vertebrae become larger and have grater BMD (L₁<L₂<L₃), and T-scores of individual vertebrae should be within approximately 1SD of each other. This observation does not apply to the hip, where differences greater than 1SD between regions may occurs because of different rates of loss cancellous and cortical bone from different hip sites.¹⁵⁵

Automated analysis of spine scans in enhanced with the introduction of computer-aided densitometry, a software feature that assists physicians in the indentification of concealed osteoporosis or osteopenia in spine scans adversely affected by conditions that cause an artificial elevation in BMD.

Material and Methods:

The study was conducted in the Department of Medicine, Rajshahi Medical College Hospital from October 2005 to July 2006. 30(thirty) male and 30(thirty) female (total 60) patient’s were studied whose ages were >45years, H/O menopause >2years, low back pain, no pathological fracture of bone. Detailed history was taken from the patient’s. They were examined physically and requisite investigations were done. Their age, sex, occupation, height, weight, and special attention was given to the back pain, morning stiffness for at least 1 hour, heat intolerance, appetite, and alteration of bowel habit.

They were also asked about past history and drug history specially prednisolone, personal history specially smoking, family history especially non traumatic fracture of bone of their mother, any history of hypertension, diabetes mellitus.

During physical examination, along with examination of the locomotor system, general physical examination and a brief examination of all other systems also were done.

Plain X-ray of the lumbar spines and hip were done in all patient’s, using DEXA Bone Densitometer (XR36, Norland, USA), the spines and proximal femurs were studied in all patient’s. The results were then compared with the reference population data for individuals of the same age, sex, and ethnic background. The comparison was verified by age matched (Z-score) and Young reference (T-score). The interpretation was done by computer generated soft ware program following WHO recommendation (Table-4).

Table: 4 World Health Organization Definitions of osteoporosis based on Bone Density levels.

Normal	Bone density within 1SD (+1SD or – 1SD) the young adult mean.
Low Bone mass (Osteopenia)	Bone density within 1 to 2.5 SD (-1SD or – 2.5SD) below the young adult mean.
Osteoporosis	Bone density 2.5 SD or more (> – 2.5 SD) below the young adult mean.
Severe Osteoporosis	Bone density more than 2.5 SD below the young adult mean and there have been one or more osteoporotic fractures.

Completed blood count was done in all patient’s, other investigation like serum calcium level, urinary calcium level, serum albumin, X-ray skull, urinary benze Jones protein, and other necessary investigations were done in relevant cases to exclude secondary causes of osteoporosis.

Results:

Among the 60 cases, the mean age incidence was 58years, the youngest patient was 45 years and the oldest patient was 81 years. The maximum of cases were found in their 7^th decades. The result is shown in Table-5.

In male patient’s, the maximum number of patient’s was in age group 60 & up years and also in female patient’s, the maximum number of patient’s, was in age group 60 & above years. This is shown in Table-6.

Among the 60 cases, the mean height incidence was 163.1 cm. The maximum number of cases was found in height group (cm) 160-169. This is shown in Table-7.

In male group, maximum number of patient’s, was in height group (cm) 160 –169; also in female group, the maximum number of patient’s was in height group (cm) 160 –169. This is shown in Table-8.

Among the 60 cases, the mean weight was 51.2 kg, the lowest weight was 30 kg, and the highest weight was 87 kg. The maximum number of cases was found in <50kg group. This is shown in the Table-9.

In male patient’s group, the maximum number of patient’s was in weight group <50 kg & also, the maximum number of patient’s, in female group, was in weight group <50 Kg. This is shown in Table-10.

Among 60cases, the mean Body mass Index (BMI) was 19.7kg/m² The highest BMI was 33.1kg/m² and the lowest BMI was 13 kg/m². The maximum number of cases was found in BMI group<18.5 kg/m². This is shown in Table-11.

In male group, the maximum number of patient’s were in BMI group 18.5 – 24.9, where as in female group, the maximum of patient’s were in BMI group <18.5. This is shown in Table-12.

Among 60 cases, 16 cases from urban and 44 cases from rural. This is shown in Table-13.

Both male and female patient’s were maximum from rural group. This is shown in Table-14.

Among 60 cases, incidence of bone mineral losses, was maximum in poor socioeconomic condition. This is shown in Table-15.

Maximum incidence of bone mineral losses among male and female groups, were also in poor socioeconomic conditions. This is shown Table-16.

Among 30 female patient’s, all of their occupations were house, wife, but in male patient’s, the incidence was maximum in other’s occupation (like landlord). This is shown in Table-17.

Among 30 male patient’s, 23 (76.7%) were smoker & among 30 female patient’s, 1 (3.3%) were smoker.  This is shown in Table-18.

No male patient’s had history of non traumatic fracture of the bone of their mothers. But among female patient’s, only eight patients had history of non-traumatic fracture of bone of their mothers. This is shown in Table-19.

Among male patient’s, only 1 patient had diabetes mellitus, and among female patient’s only 1 patient had diabetes mellitus. This is shown in Table-20.

Among 30 female patient’s, maximum patient’s were in 5-10 years group of menopausal durations. This is shown in Table-21.

Among 60 patient’s, the maximum patient’s were in back pain duration >1year. This is shown in Table-22.

Among male patient’s, maximum 19 patients had back pain duration >1year and among female patients, maximum 16 patient’s had back pain duration < 1 year. This is shown in Table-23.

The bone mineral densities are shown in Table-24. Four patient’s (male-3; Female-1) were found to have normal bone density, whereas the rest 56 patient’s had shown different grades of bone mineral loss. Among the 56 patient’s, 17 patient’s (Male-10; Female-7) suffered from osteopenia. Fourteen patients (Male-4; Female-10) had shown osteoporosis in both femoral neck and lumbar vertebra. The rest 25 patient’s (Male-13; Female-12) had shown combined osteopenic & osteoporotic changes either in lumber vertebra and / or femur. This is shown in Table-25.

BMD was higher in all sites in male than female. Osteophytes, which were common in older people, may have influenced lumber spine BMD result. This is shown in Table-26.

Among 4 normal BMD presentation patient’s, 1(25%) was in 50-54 years group & 2 (50%) were in 55-59 years group & 1 (25%) was in 60 & up years group. Among 17 osteopenic BMD presentation patient’s, 8 (47%) were in 45-49 years group & 1 (5.9%) was in 50-54 years group & 3 (17.6%) in 55-59 years group & 5 (29.4%) in 60 & up years group. Among 14 osteoporotic BMD presentation patient’s, 1 (7.1%) in 55-54 years group, & 1 (7.1%) in 55-59 years group & 12 (85.7%) in 60 & up years group. Among 25 combined BMD presentation patient’s, 2 (8%) in 45-49 years group & 5 (20%) in 50-54 years group & 6 (24%) in 50-59 years group & 12 (48%) in 60 and up years group. This is shown in Table-27.

Among 4 normal BMD presentation patient’s, 1 (25%) in 50-59 kg group & 3 (75%) in 60-69 kg group. Among 17 osteopenic BMD presentation patietns, 5 (29.4%) in < 50kg group & 4 (23.5%) in 50-59 kg group & 4 (23.5%) in 60-69kg group & 4 (23.5%) in 70 & up kg group. Among 14 osteoporotic BMD presentation patient’s, 11 (78.6%) in <50kg group & 3 (21.4%) in 50-59kg group & among 25 combined BMD presentation patient’s, 16 (64%) in<50kg group & 5 (20%) in 50-59 kg group & 3 (12%) in 60-69 kg group & 1 (4%) in 70 & up kg group. This is shown in Table-28.

Among 60 patient’s, 1 (25%) normal BMD presentation patient’s was in 150 –159 cm group & 3 (75%) were in 160 –169 cm group. 3 (17.6%) osteopenic BMD presentation patient’s are in height group 150-159 & 11(64.7%) osteopenic BMD presentation patient’s are in height group 160 –169 cm & 3 (17.6%) osteopenic BMD presentation patient’s are in height group 170 & up cm group. In osteoporotic BMD presentation patient’s, 1 (7.1%) are in height group <150cm, & 5(35.7%) are in height group 150-159 cm group, & 7 (50%) are in 160-169 cm & group, & 1 (7.1%) are in height group 170 & up cm. In Combined BMD presentation patient’s group, 5 (20%) are in height group 150-159cm, and 16 (64%) are in height group 160-169 cm, & 4 (16%) are in height group 170 & up cm. This is shown in Table-29.

In normal BMD presentation patient’s, 2 (50%) have BMI in 18.5-24.9 kg / m²  group, & 2 (50%) have BMI in 25-29.9 kg/m² group. In osteopenic BMD presentation patient’s 3 (17.6%) patient’s BMI in < 18.5kg/m² group, and 10 (58.8%) in 18.5-24.9kg/m² BMI group, & 2 (11.8%) in 25-29.9 kg/m² BMI group & 2 (11.8%) in 30 & up kg/m² BMI group. In osteoporotic BMD patient’s, 11(78.1%) in < 18.5kg/m² BMI group & 3 (21.4%) in 18.5-24.9kg/m² BMI group. In combined BMD presentation patient’s, 13 (52%) in < 18.5kg/m² BMI group & 11 (44%) in 18.5 –24.9kg/m² BMI group & 1 (4%) in 25-29.9kg/m² BMI group. This is shown in Table-30.

In normal BMD presentation patient’s, 1 (25%) are poor & 3 (75%) are in middle class. In osteopenic BMD presentation patient’s, 10 (58.8%) are poor & 6 (35.3%) are in middle class & 1 (5.9%) are in rich group. In osteoporotic BMD presentation patient’s, 8 (57.2%) are poor & 5 (35.7%) are in middle class & 1 (7.2%) are in rich group. In combined BMD presentation patient’s, 14 (56%) are poor & 11 (44%) are middle class. This is shown in Table-31.

Among 30 female patient’s, all were housewives. Among 30 male patient’s, in normal BMD presentation patient’s, 1 (33.3%) patient’s occupation was service & 2 (66.7%) patient’s occupation were others. In osteopenic BMD presentation male patient’s 1(10%) patient occupation was labor & also same number patient occupation, is business & 8 (80%) patient’s occupation were others. In osteoporotic BMD presentation male patient’s, 2 (50%) patient’s occupation were business & also same number of patient’s occupations was other. In combined BMD presentation male patient’s, 2 (15.4%) patient’s occupation were labor & also same number of patient’s occupation were service, business & 7 (53.8%) patient’s occupation were others. This is shown in Table-32.

Among 60 patient’s, in normal BMD presentation patient’s, 2 (50%) patient’s were in urban & 2 (50%) patient’s were in rural. In osteopenic BMD presentation patient’s, 4 (23.5%) were in urban & 13 (76.5%) patient’s were in rural. In osteoporotic BMD presentation patient’s, 3 (21.4%) patient’s were in urban & 11 (78.6%) patient’s were in rural. In combined BMD presentation patient’s, 7(28%) patient’s were in urban & 18 (72%) patient’s were in rural. This is shown in Table-33.

In normal BMD presentation patient’s, 2(50%) have smoking history. In osteopenic BMD presentation patient’s, 8 (47%) have smoking history. In osteoporotic BMD presentation patient’s, 4 (28.6%) have smoking history. In combined BMD presentation patient’s, 10(40%) have smoking history. This is shown Table-34.

Among 30 male patient’s, none of them have family history (non traumatic fracture of the bone of their mother). But among 30 female patient’s, in osteopenic BMD presenting female patient’s, 2 (28.6%) patient’s have family history positive. In osteoporotic BMD presenting female patient’s, 1 (10%) have family history positive. In combined BMD presenting female patient’s, 5 (41.7%) patient’s have family history positive. This is shown in Table-35.

Among the 60 patient’s, 2 patient’s were diabetic. In the normal BMD presetting patient’s 01 (25%) patient is diabetic, which is 25%, and in combined BMD presenting patient’s, 1(4%) patient is diabetic. So, incidence of diabetics with normal BMD presenting patient’s is higher. This is shown in Table-36.

Among the 30 female patient’s, normal BMD presenting patient’s, 1 (100%) patient menopause duration was 5-10years group. In osteopenic BMD presenting female patient’s, 4 (57.1%) patient’s menopausal duration was < 5years group and 2 (28.6%) patient’s menopausal duration was 5-10years group and 1(14.3%) patient’s menopausal duration was 10 & up years group in osteoporotic BMD presenting female patient’s, 3 (30%) patient’s menopausal duration was 5-0 years group, and 7 (70%) patient’s menopausal duration was 10 & up years group. In combined BMD presenting female patient’s, 2 (16.7%) patient’s menopausal duration was <5years group & 7 (58.3%) patient’s menopausal duration was 5-10 years group, & 3 (25%) patient’s menopausal durations was 10 & up years group. This is shown in Table-37.

In normal BMD presenting patient’s, 2 (50%) patient’s back pain duration was <1 year group, & 2 (50%) patient’s back pain duration was >1 year group. In osteopenic BMD presenting patient’s, 9(52.9%) patient’s back pain duration was <1year group, & 8 (47%) patient’s back pain duration was >1year. In osteoporotic BMD presenting patient’s, 6(42.8%) patient’s back pain duration was <1year group, & 8(57.2%) patient’s back pain duration was> 1year group. In Combined BMD presenting patient’s, 10(40%) patient’s back pain duration was < 1year group, & 15 (60%) patient’s back pain duration was > 1year group. This is shown in Table-38.

In normal BMD presenting patient’s, 25% have systolic blood pressure was < 140mm of Hg and 75% patient’s blood pressure were in 140-160 mm of Hg group. In osteopenic BMD presenting patient’s, 52.9% patient’s have systolic B.P. <140 mm of Hg group and 47.1% patient’s have systolic B.P. in 140-160 mm of Hg group. In osteoporotic BMD presenting patient’s, 57.1% paitents have systolic B.P.  was < 140 mm of Hg group and 42.9% patient’s have systolic B.P was 140 –160 mm of Hg group. In combined BMD presenting patient’s, 48% patient’s systolic B.P. equally was in < 140 mm of Hg and 140 – 160 mm of Hg group and 4% patient’s systolic B.P. was in > 160mm of Hg group. This is shown in Table-39.

In normal BMD presenting patient’s, 25% patient’s diastolic B.P. was in <90mm of Hg & 75% patient’s diastolic B.P was in 90-100 mm of Hg group. In osteopenic BMD presenting patient’s, 82.4% patient’s diastolic B.P. was in <90mm of Hg & 17.6% patient’s diastolic B.P was in 90-100 mm of Hg group. In osteoporotic BMD presenting patient’s, 71.4% patient’s diastolic was < 90 mm of Hg group & 28.6% patient’s diastolic B.P was in 90-100 mm of Hg group. In combined BMD presenting patient’s, 76% patient’s diastolic B.P was in < 90mm of Hg group & 24% patient’s diastolic BP was in 90-100 mm of Hg group. This is shown in Table-40.

Among the male patient’s, 24(80%) patient’s have degenerative changes and 4(13.3%) patient’s have osteoporotic changes and 2 (6.7%) patient’s have normal finding on X-ray L-S spine. In female patient’s, 3 (10%) have normal finding and 9(30%) patient’s have osteoporotic changes & 10 (30.3%) patient’s have degenerative changes and 8 (26.7%) patient’s have combined changes on X-ray L-S spine. This is shown in Table-41.

Sensitivity of the X-ray in assessing BMD is 39%. This is shown in Table-42.

Table- 5

Age incidence

Total patient’s = 60

Age group (years)	Number of Patient’s	Percentage
45 – 49	10	16.7%
50 – 54	8	13.3%
55 – 59	12	20%
60 & up	30	50%

Table-6

Age incidence between male & female group

Age group (years)	45 – 49		50 – 54		55 – 59		60 & up
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Male       No =30	6	20	4	13.3	2	6.7	18	60
Female No= 30	4	13.3	4	13.3	10	33.3	12	40

Table-7

Height incidence

Total patient’s=60

Height group (cm)	Number of Patient’s	Percentage
< 150	1	1.7%
150 – 159	14	23%
160 – 169	37	61%
170 & up	8	13%

Table-8

Height incidence between male & female group

Height group (cm)	< 150		150 – 159		160 – 169		170 & up
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Male       No =30			5	16.7	17	56.7	8	26.7
Female No= 30	1	3.3	9	30	20	66.7

Table-9

Weight incidence

Total patient’s=60

Weight group (kg)	Number of Patient’s	Percentage
< 50	32	53.3%
50 – 59	13	21.7%
60 –69	10	16.7%
70 & up	5	8.3%

Table-10

Weight incidence between male & female group

Weight group (kg)	< 50		50 – 59		60 – 69		70 & up
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Male       No =30	13	43.3	8	26.7	6	20	3	10
Female No= 30	19	63.3	5	16.7	4	13.3	2	6.7

Table-11

BMI incidence

Total patient’s=60

BMI group (kg/m2)	Number of Patient’s	Percentage
< 18.5	27	45%
18.5 – 24.9	26	43.3%
25 –29.9	5	8.3%
30 & up	2	3.3%

Table-12

BMI incidence between male & female group

BMI group (kg/m2)	<18.5		18.5 – 24.9		25 –29.9		30 & up
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Male       No =30	12	40	13	43.3	4	13.3	1	3.3
Female No= 30	15	50	13	43.3	1	3.3	1	3.3

Table-13

Address incidence

Total patient’s 60

Address	Number of Patient’s	Percentage
Urban	16	26.7%
Rural	44	73.3%

Table-14

Address incidence between male & female group

Address	Urban		Rural
	No of pt	%	No of pt	%
Male       No =30	5	16.7	25	83.3
Female No= 30	11	36.7	19	63.3

Table-15

Incidence in different socioeconomic condition

Total patient’s=60

Socioeconomic condition	Number of Patient’s	Percentage
Poor	33	55%
Middle Class	25	41.7%
Rich	2	3.3%

Table-16

Socioeconomic incidence between male & female group

Socioeconomic condition	Poor		Middle Class		Rich
	No of pt	%	No of pt	%	No of pt	%
Male       No =30	17	56.7	12	40	1	3.3
Female No= 30	16	53.3	13	43.3	1	3..3

Table-17

Occupational Status in male patient’s

 

Occupation	Number of patient’s (No =30)	Percentage (%)
Labor	3	10%
Service	3	10%
Business	5	16.7%
Others	19	63.3%

 

Table-18

Smoking incidence in different sexes

Patient’s	Number of patient’s	Percentage (%)
Male               No = 30	23	76.7%
Female          No = 30	1	3.3%

Table-19

Family history incidence

Patient’s	Family history positive	Percentage (%)
Female          No = 30	8	26.7

Table-20

Patient’s	Diabetic history	Percentage (%)
Male               No = 30	1	3.3%
Female          No = 30	1	3.3%

Table-21

Menopausal duration incidence

Menopausal duration (Years)	Number of Patient’s	Percentage
<5	6	20%
5 – 10	13	43.3%
10 & up	11	36.7%

Table-22

Back pain duration incidence

Back pain duration (Years)	Number of Patient’s	Percentage (%)
< 1	27	45%
> 1	33	55%

Table-23

Back pain duration incidence in different sexes

Back pain duration (Years)	< 1		> 1
	No of pt	%	No of pt	%
Male       No =30	11	36.7	19	63.3
Female No= 30	16	53.3	14	46.7

Table-24

Bone mineral density (in gm/cm²) of lumbar vertebrae

and femoral neck in different categories.

	Normal No = 4		Osteopenia No = 17		Osteoporosis No = 14		Combined                    No = 25
							Osteopenia		Osteoporosis
Site	LV	FN	LV	FN	LV	FN	LV	FN	LV	FN
BMD (SD)	1.2000 .05	1.0128 .02	.8396 .03	.7731 .06	.5860 .04	.5976 .03	.8250 .03	.8170 .01	.5484 0	.6502 .03
T-Score (SD)	.73 .07	.48 .01	1.56 .02	1.88 .05	3.19 .01	3.52 .01	1.73 .01	2.05 .02	3.42 0	3.26 .09

* LV = lumbar vertebrae; FN= Femoral Neck; * Combined= Osteoporosis + osteopenia.

Table-25

Bone Mineral losses in different sexes.

Patient’s	Normal No = 4		Osteopenia No = 17		Osteoporosis No = 14		Combined No = 25
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Male       No=30	3	10	10	33.3	4	13.3	13	43.3
Female No=30	1	3.3	7	23.3	10	33	12	40

Table-26

Comparison of male (M) and female (F) population for lumbar spine and femoral neck bone mineral densities stratified by age groups.

Age (years)	No	Spine (gm/cm2) [mean SD]	Femur (gm/cm2) [mean SD]
45 – 49	M (6)	.9043 .09	.8432  .08
	F (4)	.8850  .14	.7654  .07
50 – 54	M (4)	.9840 .16	.9147  .12
	F (5)	.7497  .18	.6602  .07
55 – 59	M (2)	.9076 .004	.7697  .01
	F (9)	.7912  .21	.6984  .01
60  & up	M (18)	.8470 .19	.7440  .16
	F (12)	.6387  .15	.5737  .08

Table-27

Association with age

Presentation	45 – 49 years		50 – 54 years		55 – 59 years		60 & up years
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Normal           No=4			1	25	2	50	1	25
Osteopenia     No=17	8	47	1	5.9	3	17.6	5	29.4
Osteoporosis  No=14			1	7.1	1	7.1	12	85.7
Combined       No=25	2	8	5	20	6	24	12	48

Table-28

Association with weight

Presentation	< 50 kg		50 – 59 kg		60 – 69 kg		70 & up kg
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Normal           No=4			1	25	3	75
Osteopenia     No=17	5	29.4	4	23.5	4	23.5	4	23.5
Osteoporosis  No=14	11	78.6	3	21.4
Combined       No=25	16	64	5	20	3	12	1	4

Table-29

Association with Height

Presentation	< 150 cm		150 – 159cm		160 – 169 cm		170 & up cm
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Normal           No=4			1	25	3	75
Osteopenia     No=17			3	17.6	11	64.7	3	17.6
Osteoporosis  No=14	1	7.1	5	35.7	7	50	1	7.1
Combined       No=25			5	20	16	64	4	16

Table-30

Association with BMI

Presentation	< 18.5 kg/m2		18.5 – 24.9 kg/m2		25 – 29.9 kg/m2		30 & up kg/m2
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Normal           No=4			2	50	2	50
Osteopenia     No=17	3	17.6	10	58.8	2	11.8	2	11.8
Osteoporosis  No=14	11	78.6	3	21.4
Combined       No=25	13	52	11	44	1	4

Table-31

Association with Socioeconomic condition

Presentation	Poor		Middle Class		Rich
	No of pt	%	No of pt	%	No of pt	%
Normal           No=4	1	25	3	75
Osteopenia     No=17	10	58.8	6	35.3	1	5.9
Osteoporosis  No=14	8	57.2	5	35.7	1	7.2
Combined       No=25	14	56	11	44

Table-32

Association with Occupation

Presentation	Labor		Service		Business		Others
	No of pt	%	No of pt	%	No of pt	%	No of pt	%
Normal           No=3			1	33.3			2	66.7
Osteopenia     No=10	1	10			1	10	8	80
Osteoporosis  No=4					2	50	2	50
Combined       No=13	2	15.4	2	15.4	2	15.4	7	53.8

Table-33

Association with address

Presentation	Urban		Rural
	No of pt	%	No of pt	%
Normal             No=4	2	50	2	50
Osteopenia        No=17	4	23.5	13	76.5
Osteoporosis     No=14	3	21.4	11	78.6
Combined         No=25	7	28	18	72

Table-34

Association with Smoking

Presentation	No of pt	%
Normal             No=4	2	50
Osteopenia        No=17	8	47
Osteoporosis     No=14	4	28.6
Combined         No=25	10	40

Table-35

Association with Family history

Presentation	No of pt	%
Normal             No= 1
Osteopenia        No= 7	2	28.6
Osteoporosis     No= 10	1	10
Combined         No= 12	5	41.7

Table-36

Association with D.M.

Presentation	No of pt	%
Normal             No= 4	1	25
Osteopenia        No= 17	0	0
Osteoporosis     No= 14	0	0
Combined         No= 25	1	4

 

Table-37

Association with duration of menopause

Presentation	< 5 years		5 – 10 years		10 & up years
	No of pt	%	No of pt	%	No of pt	%
Normal           No=1			1	100
Osteopenia     No=7	4	57.1	2	28.6	1	14.3
Osteoporosis  No= 10			3	30	7	70
Combined       No= 12	2	16.7	7	58.3	3	25

Table-38

Association with duration of back pain

Presentation	< 1 Year		> 1 Year
	No of pt	%	No of pt	%
Normal             No=4	2	50	2	50
Osteopenia        No=17	9	52.9	8	47
Osteoporosis     No=14	6	42.8	8	57.2
Combined         No=25	10	40	15	60

 

Table-39

Relation with systolic BP

Presentation	< 140  mm of Hg		140 – 160 mm of Hg		> 160  mm of Hg
	No of pt	%	No of pt	%	No of pt	%
Normal           No=4	1	25	3	75
Osteopenia     No=17	9	52.9	8	47.1
Osteoporosis  No=14	8	57.1	6	42.9
Combined       No=25	12	48	12	48	1	4

Table-40

Relation with diastolic BP

Presentation	< 90  mm of Hg		90 – 100 mm of Hg		> 100  mm of Hg
	No of pt	%	No of pt	%	No of pt	%
Normal           No=4	1	25	3	75
Osteopenia     No=17	14	82.4	3	17.6
Osteoporosis  No=14	10	71.4	4	28.6
Combined       No=25	19	76	6	24

Table-41

X- ray finding in different sexes.

Patient’s	X-ray L-S spine
	Normal		Osteoporotic changes		Degenerative changes		Combined (Both Osteo. + Degen. Changes)
	No. of pt.	%	No. of pt.	%	No. of pt.	%	No. of pt.	%
Male        No =30	2	6.7	4	13.3	24	80
Female    No =30	3	10	9	30	10	33.3	8	26.7

 

Table-42

X-ray finding	Bone loss found in BMD	No bone loss found in BMD
Positive scan	20	1
Negative scan	31	8
	51	9

Discussion:

The present study was under taken in elderly patient’s presenting with low back pain to evaluate the frequency of osteoporotic changes in skeleton and to evaluate the sensitivity of radiology for assessing bone density in medicine units of Rajshahi Medical College Hospital from 12-10-2005 to 16-07-2006. A total 60 cases were studied. Among them 30 patient’s were male & 30 patient’s were female. In this series, the peak incidence of bone mineral losses occurred in 60 & up year’s age group. Next age group was 55-59 years. 50% of patient’s in 60 & up year’s age group and 20% of patient were 55-59 years age group. In male patient’s, highest 60% were in 60 & up years age groups, 2^nd highest 20% were in 45-49 years age group, In female patient’s, highest 40% were in 60 & up years age group, second highest 33.3% were in 55-59 years age group. The youngest patient was 45 years and oldest patient was 81 years. On the basis of many epidemiologic clinical and laboratory findings, Riggs and his colleagues have proposed that evolutional osteoporosis is divided in to two major and distinct syndromes, ie, Type- I : post menopausal osteoporosis & Type – II : Age related osteoporosis.¹⁶⁸ This study is very much similar to the mentioned categories. ¹⁶⁸

Mean height was 163.1cm. Maximum patient’s was in 160-169cm group. Next height number of patient’s was in 150-159 cm group. So 61% patient’s were in 160-169cm height group, & 23% patient’s were in 150-159cm height group. In male patient’s, highest 56.7% were in 160-169 cm height group and next 26.7% of patient’s were in 170 & up cm height group and patient’s in < 150cm height group. In female patient’s, highest 66.7% of patient’s also were in 160-169 cm height group and next 30% of patient’s were in 150-159cm height group and no patient in 170 and up cm height group.

Normal BMD presentation patient’s group, 75% were in 160-169 cm weight group and next 25% were in 150-159cm group. In osteopenic BMD presenting patient, highest 64.7% were in 160-169cm group & next highest 17.6% were in equally in 150-159 cm & 170 and up cm groups. In osteoporotic BMD presenting patient’s, highest 50% were in 160-169 cm group & next 35.7% were in 150-159cm group and 7.1% were equally in < 150 cm & 170 & up cm groups. In combined BMD presenting patient’s, highest 64% patient’s were in 160-169 cm group and next highest 20% were in 150-159cm group. So there is association between the height and bone mineral losses.^{118, 119}

The maximum number patient’s was in < 50kg weight group. Next maximum number of patient’s was in 50-59kg weight group. So 53.3% were in <50kg group and 21.7% were in 50-59kg group. In male patient’s 43.3% were in <50kg group & next highest 26.7% were in 50-59kg group. In female patient’s, highest 63.3% were in <50kg group and next 16.7% were in 50-59 kg group. In normal BMD presenting patient’s, 75% were in 60-69kg group and next 25% were in 50-59kg group. In osteopenic BMD presenting patient’s maximum 29.4% were in <50kg group and next 23.5% were equally distributed to the rest of the groups. In osteoporotic BMD presenting patient’s, highest 78.6% were in <50kg group and in combined BMD presenting patient’s, highest64% were in <50kg group. So there is positive relationship between weight & bone mineral density.^{120, 127, 169.}

The maximum of patient’s BMI were in < 18.5kg /m² group & next highest number of patient’s were in 18.5 –24.9kg/m² group. 45% were in < 18.5kg/m² group and next highest 43.3% were in 18.5-24.9 kg /m². In male patient’s, 43.3% group were in 18.5-24.9kg/m² and next highest 40% were in <18.5 kg /m² group. In Female patient’s, highest 50% were in <18.5kg/m² group and next highest 43% were in 18.5-24.9 kg/m² group. In normal BMD presenting patient’s, 50% equally in 18.5-24.9 kg/m² and 25-29.9 kg/m² groups. In osteopenic BMD presenting patient’s, maximum 58.8% were in 18.5-24.9 kg/m² group and next highest 17.6% were in <18.5 kg/m². In osteoporotic BMD presenting patient’s, maximum 78.6% were in < 18.5% kg/m² group and next 21.4% were in 18.5-24.9 kg/m² group. In combined BMD presenting patient’s, highest 52% were in <18.5 kg/m² group & next highest 44% were in 18.5-24.9 kg/m² group. So body mass index (BMI) has positive correlation with bone mineral density which is consistent with the study by C.A.F. Zerbini et all from Brazil (2000).¹⁷⁰

Highest number of patient 44 (73.3%) from rural, and 16 (26.7%) from urban. In male patient 25(83.3%) from rural and in female patient’s 19(63.3%) from rural. In normal BMD presenting patient’s, 50% equally from urban & rural. In osteopenic BMD presenting patient’s, 76.5% from rural, & 23.5% from urban. In osteoporotic BMD presenting patient’s, 78.6% from rural & 21.4% from urban. In combined BMD presenting patient’s, 72% from rural & 28% from urban. So in rural population, bone mineral losses higher than urban population.

Highest number 33 (55%) patient’s are poor, and then 25(41.7%) patient’s are in middle class. In male patient’s, 56.7% patient’s are poor and then 40% patient’s are in middle class. In female patient’s, 53.3% patient’s are in poor & then 43.3% patient’s are in middle class. In normal BMD presenting patient’s, 75% patient’s are in middle class and 25% patient’s are in poor. In osteopenic BMD presenting patient’s, 58.8% are in poor and 35.3% patient’s are in middle class. In osteoporotic BMD presenting patient’s, highest 75.2% patient’s are poor and than 35.7% patient’s are in middle class. In combined BMD presenting patient’s, 56% are poor & then 44% patient’s are in middle class. So in poor socioeconomic condition, bone mineral losses is high, which in consistent with the study by May-Choowang, et all from USA (2006).¹⁷¹

All female patient’s occupation were housewife. But in male patient’s, others (like land lord) occupation were 63.3% & 16.7% patient’s occupation were business & 10% patient’s occupation equally were labor & service. In normal BMD presenting male patient’s, 66.7% patient’s occupation were others & 33.3% patient’s occupation were service. In osteopenic BMD presenting patient’s, 80% patient’s occupation were others and 10% patient’s occupation equally were business and labor. In osteoporotic BMD presenting male patient’s, 50% patient’s occupation were others and 50% patient occupation were business. In combined BMD presenting male patient’s, 53.8% patient’s occupation were other’s and 15.4% patient’s occupation equally were labor, service and business. So BMD losses marked in other’s occupation patient’s, in which occupation physical labor is minimal.³² So BMD has positive correlation with physical activity which is consistent with the study by Alex A. Florindo, et al from Brazil (2002)¹⁷²

None of the male patient’s have family history positive. Among female patient’s, only 26.7% patient’s have family history of nontraumatic fractures of bones. In osteopenic BMD presenting patient’s, only 28.6% female patient’s family history positive. In osteoporotic BMD presenting female patient’s, only 10% patient’s have family history positive. In combined BMD patient’s 41.7% patient’s have family history positive. So, those who are family history positive, much of them in combined BMD that is either osteoporosis of lumber vertebra and osteopenia of femoral neck or osteoporosis femoral neck and osteopenia of lumber vertebra. This study consistent with the study by Eric S. Orwoll, et all in 1996.¹⁷³

Among male patient’s, only 3.3% of patient’s have D.M. & among female patient’s, only 3.3% patient, have D.M. In normal BMD presenting patient’s, 25% patient’s have D.M. and in combined BMD presenting patient’s, only 4% patient’s have D.M. So there is no association between BMD & D.M. This study is consistent with the study by M. Sert, et all in 2003.¹⁷⁴

Among the male patient’s, 76.7% patient’s are smokers and only among female patient’s, only 3.3% patient’s are smokers. In normal BMD presenting patient’s, 50% patient’s are smokers. In osteopenic BMD presenting patient’s, 47% patient’s are smokers. In osteoporotic BMD presenting patient’s, only 28.6% patient’s are smokers. In combined BMD presenting patient’s, 40% patient’s are smokers. So there is no significant relation between smoking and BMD. In 1994, H May, el al in U.K. also shown that there is no significant relation between smoking and BMD.¹⁷⁵

Among female patient’s, 43.3% patient’s menopausal duration are 5-10 years group. Next highest 36.7% female patient’s menopausal duration are 10 and up years group. In normal BMD presenting patient’s, 100% are in 5-10 years group. In osteopenic BMD presenting patient’s, highest 57.1% patient’s are in <5years menopausal duration group and next 28.6% patient’s are in 5-10 years menopausal duration group. In osteoporotic BMD presenting patient’s, maximum 70% patient’s are in 10and up years menopausal duration group and next 30% patient’s are in 5-10 years menopausal duration group. In combined BMD presenting patient’s, 58.3% patient’s are in 5-10 years menopausal duration group and next maximum 25% patient’s are in 10 and up years menopausal duration group. So there is negative association beteen BMD and menopausal duration. S. Chowdhury, et al (2001) from Dhaka also got negative association between BMD and menopausal duration.¹⁶⁹

45% patient’s back pain duration <1years group & 55% patient’s back pain duration> 1 year. In male patient’s, 63.3% patient’s back pain duration > 1years group and only 36.7% patient’s back pain duration <1year.  In female patient’s, 53.3% patient’s back pain duration < 1years group and 46.7% patient’s back pain duration are in > 1year group. In normal BMD presenting patient’s, 50% patient’s are equally distributed in both groups. In osteopenic BMD presenting patient’s, 52.9% patient’s are in <1year back pain group. In osteoporotic BMD presenting patient’s, 57.2% patient’s are in >1year back pain group. In combined BMD presenting patient’s, 60% patient’s are in > 1year back pain duration group. So there is an positive association between BMD and back pain duration. Takashi Manabe in 2003 have shown that there is positive relation between BMD and back pain.¹⁷⁶

In normal BMD presenting patient’s, 25% patient’s have systolic B.P. <140mm of Hg and 75% patient’s have systolic B.P. 140-160 mm of Hg. group. In osteopenic BMD presenting patient’s, 52.9% patient’s have systolic B.P. < 140 mm of Hg and 47.1% patient’s have systolic B.P. in 140-160mm of Hg. In osteoporotic BMD presenting patient’s, 57.1% patient’s have systolic B.P. < 140mm of Hg group and 42.9% patient’s have systolic B.P. 140 –160 mm of Hg. In combined BMD presenting patient’s, 48% patient’s systolic equally in <140mm of Hg and 140-160mm of Hg. group and 40% patient’s have systolic B.P. in >160 mm of Hg. group. So there is no association between systolic B.P. and BMD.

In normal BMD presenting patient’s, 25% patient’s have diastolic B.P. <90mm of Hg and 75% patient’s have diastolic B.P. in 90-100 mm of Hg. group. In osteopenic BMD presenting patient’s, 82.4% patient’s have diastolic B.P. < 90 mm of Hg and 17.6% patient’s have diastolic B.P. in 90-100mm of Hg. In osteoporotic BMD presenting patient’s, 48% have diastolic B.P. equally distributed in < 90mm of Hg and 90-100 mm of Hg groups and 4% patient’s have diastolic B.P. >160 mm of Hg groups. So there is no association between diastolic B.P. and BMD.  But E. A. Jan Kowska, et al in 2002 have shown that there is no relationship between BMD and systolic B.P., but inverse relationship between BMD and diastolic B.P.¹⁷⁷

In the present study BMD at the lumbar spine and femoral neck level was higher for men than for women in all age groups. BMD at the femoral neck level deceased for both sexes with age but reduction was lesser and later for men. BMD is higher in lumber vertebra then for femoral neck, this is because of osteophytes. This study is consistent with the study by C. A. F. Zerbini, et all from Brazil (2002).¹⁷⁰ Radiology is of limited value unless there is severe bone loss or compression fracture occur. Radiology is the least sensitive method for assessing for bone density. This study is consistent with the study by selim M Ansari, et all from Bangladesh (2002).¹⁷⁸

Summary and Conclusion: 

A series of 60 cases were studied which included 30 male & 30 female elderly patient’s presenting with low back pain in medicine units of Rajshahi Medical College Hospital, Rajshahi. The mean age of the patient was 58 years. Maximum number of patient’s height is 160-169cm group. Maximum number of patient’s weight were <50kg (male>female) in weight. 50%female & 40% male patient’s BMI were <18.5kg /m². About 73.3% patient’s were from rural origin. Maximum patient’s were poor. About 76.7% male patient’s were smoker. Females were housewives and most male patient’s occupation were different. Only 26.7% female patient’s had family history of nontraumatic fracture of bones of their mothers. Most of the female patient’s menopausal duration was >5 years.  Maximum female patient’s back pain duration was <1year and maximum male patient’s back pain duration was >1year. Maximum male patient’s presented as either osteopenic of combined BMD and maximum female patient’s either osteoporotic or combined (osteoporosis of the lumber vertebra and osteopenia of the femoral neck or osteoporosis of the femoral neck and osteopenia of the lumber vertebra). There was an inverse relationship between BMD and the age. There was an positive relationship between weight and BMD. Body mass index (BMI) had positive relation with the BMD. Bone mineral losses were high in poor socioeconomic condition. In male patient’s BMD losses marked in other’s type occupation, in which physical labor was minimal. Bone mineral losses were higher in rural population than urban population. Those who had family history that is history of nontraumatic fracture of bones of their mothers, many of them had combined reduction of BMD (either osteoporosis of the lumber vertebra and osteopenia and femoral neck or osteopenia of the lumber vertebra and osteoporosis of the femoral neck) and also reduced BMD. There was no significant relation between smoking and BMD. There was also no relationship between D.M. and BMD. There was negative relationship between menopausal duration and BMD. Blood pressure (Systolic and diastolic) had no relationship with BMD. 80% male patient’s X-ray L-S spines finding was degenerative changes. But in female patient’s, X-ray finding nearly equally distributed in osteoporotic changes or degenerative changes or combined (Both osteoporotic + Degenerative changes) changes. BMD at the lumber spine and femoral neck level was higher for men than for women in all age groups. BMD at femoral neck level decreased for both sexes with age but reduction was lesser and later for men. BMD was higher in lumber vertebra than for femoral neck, this was because of osteophytes. Radiology was of limited value unless there was severe bone loss and compression fractures occurred. Radiology was the least sensitive method for assessing bone density.

We studied only a limited number of patient’s in an urban hospital setting lacking inadequate epidemiological date & works. So this study revealed many features which were not similar to real clinical situations in our country. On the other hand, western standard and styles are also different. On that ground, it may partially meet up the requirements to fill up the gap or better to say to add something to the bottomless ocean of knowledge.

Case No. 01

Md. Abul Kasem, 65 years, from Mohadebpur, Noagan, retired service man of bellow average body build and body weight, ex-smoker, non-diabetic, normotensive admitted on 26-02-2006 bed no P/3, RMCH, Rajshahi with low back pain and pain in the Rt. Knee. His loss of height was absent and morning stiffness for at least 1 hour was absent. He complained weight loss for 1 year. Heat intolerance was absent. His appetite was normal. Bowel habit was normal. His back pain had no radiation; duration was 2¹/₂ months. Pain in the Right Knee joint was sudden onset and joint was swelled up and increase hotness over the joint. He was non alcoholic, His dietary habit was average. His past history was insignificant. He did not give any family history of non traumatic fracture on bones of his parent.

On examination: he was ill looking, below average body build, with anaemia, but had no jaundice, cyanosis, clubbing & oedema. His pulse rate was 76/min, rhythm was regular, character and volume was normal. His BP was 120/65 mm of Hg.

Straight leg raising (SLR) test was negative. Examination of the Rt. Knee joint revealed that temperature was increased, tenderness present, and massage test was positive. Others systemic examination was normal.

On investigation, X-ray L-S spines showed degenerative changes in the lumber spines. BMD study done by DEXA scan, showed osteoporosis in the both hips and osteopenia of the lumbar spines. This is showed in the figure A, B, C. Blood examination showed Hb%-45%, ESR-60 mm in 1^st hour. Total count was normal & there was neutrophilia. C-RP was high. Serum calcium was 8.2mg /dl. RBS with CUS and serum creatinine were normal, S. uric acid was 8.5mg/dl. Features of the blood film and bone marrow can not be ruled out storage disease. No punch out lesion was seen on X-ray skull (lateral view). Urinary benze jones protein was negative.

The diagnosis was lumber spondylosis with osteoporosis of the both hips and osteopenia of the lumber spines and acute gout.

Case No: 02

Mrs. Lokjhan 70 years, housewife, from Durgapur, Rajshahi, poor socioeconomic condition, non-diabetic, normotensive, admitted in RMCH, Rajshahi, with the complaints of back pain. There was no radiation of pain, dull in nature, persistent in character, not aggravated by coughing, sneezing.    There was no history of morning stiffness for at least 1 hour. Loss of height, weight loss, and heat intolerance was absent. Appetite was normal. Alteration of bowel habit was absent. She was a non-alcoholic, non-smoker. Her dietary habit was average. She had no significant past illness. She had no family history of non-traumatic fracture of bones of her parent.

On examination, she was ill looking, below average body build with no anaemia, jaundice, cyanosis, clubbing, oedima. Her pulse rate was 70/min, rhythm was regular, character and volume was normal. Her BP was 110/65 mm of Hg.

Straight leg raising (SLR) test was negative. Examination of the other systems was also normal.

On investigation, X-ray L-S spines showed osteoporotic changes. Bone menial density (BMD) study done by DEXA scan showed osteoporosis of the both hips and lumber spines. This was shown in Fig. D, E, F. Blood Examination showed Hb%, ESR, TC, DC, normal & CPBF showed non-specific findings. Random blood sugar was normal.

The diagnosis was osteoporosis of the lumber spines and the both hips.