Case History: Acute Exacerbation of Chronic Bronchial Asthma

PATIENT DETAILS

CHIEF COMPLAINTS

1. Breathlessness - 2 days, worsening over past 6 hours
2. Wheeze - 2 days
3. Cough with scanty whitish sputum - 3 days
4. Chest tightness - 2 days

HISTORY OF PRESENT ILLNESS

PAST HISTORY

• Bronchial Asthma: Diagnosed 10 years ago. Multiple emergency room visits (approximately 3 per year). One hospital admission 2 years ago requiring nebulization. No prior intubation or ICU admission.
• Trigger factors identified: Dust (occupational - textile mill), cold air, viral upper respiratory infections, exercise
• Allergic Rhinitis: Present, on intermittent antihistamines
• No history of: Tuberculosis, diabetes mellitus, hypertension, cardiac disease, peptic ulcer disease, surgical procedures
• No known drug allergies

TREATMENT HISTORY

• Salbutamol MDI (200 mcg) - as needed (rescue inhaler)
• Budesonide MDI (200 mcg) BD - ran out 1 week ago, not refilled
• Montelukast 10 mg OD - compliance irregular

PERSONAL HISTORY

• Diet: Mixed (non-vegetarian)
• Appetite: Reduced since onset of illness
• Sleep: Disturbed (due to nocturnal breathlessness)
• Bowel and bladder habits: Normal
• Smoking: 10 pack-year history; quit 3 years ago
• Alcohol: Occasional
• Occupation: Textile mill worker - significant occupational dust exposure

FAMILY HISTORY

• Mother: Bronchial asthma
• Elder sister: Allergic rhinitis
• No family history of tuberculosis, malignancy, or cardiac disease

SOCIOECONOMIC HISTORY

• Lower-middle socioeconomic class (Kuppuswamy scale)
• Lives in a ground-floor urban flat; presence of house dust, carpets; no pets
• Limited access to medications due to financial constraints (explains non-refill of inhaled corticosteroid)

GENERAL PHYSICAL EXAMINATION

SYSTEMIC EXAMINATION

Respiratory System

• Chest shape: Hyperinflated (barrel-shaped appearance, increased AP diameter)
• Respiratory rate: 32/min
• Type: Predominantly abdominal breathing
• Accessory muscles of respiration in use
• Intercostal and subcostal indrawing present

• Trachea: Central
• Chest expansion: Reduced bilaterally and symmetrically
• Vocal fremitus: Decreased bilaterally

• Bilateral hyperresonance
• Cardiac dullness: Reduced
• Liver dullness: Shifted downward (hyperinflation)

• Air entry: Reduced bilaterally
• Breath sounds: Vesicular with prolonged expiratory phase
• Added sounds: Bilateral high-pitched expiratory wheeze (polyphonic sibilant rhonchi); inspiratory wheeze also present
• No crackles (rales) or crepitations
• Vocal resonance: Decreased

Cardiovascular System

• S1, S2 heard; no murmurs
• JVP not elevated
• Pulse: Tachycardic, pulsus paradoxus ~14 mmHg (significant; >10 mmHg indicates severe obstruction)

Abdomen

• Soft, non-tender
• No organomegaly
• Bowel sounds present

Central Nervous System

• Conscious, alert, oriented to time/place/person
• No focal neurological deficit
• Mild agitation due to hypoxia

INVESTIGATIONS

Bedside / Immediate

Arterial Blood Gas (ABG) - Room Air

Hematological Investigations

Biochemistry

Sputum Examination

• Gross: White, mucoid, tenacious
• Microscopy: Numerous eosinophils; Curschmann's spirals (casts of small airways); Charcot-Leyden crystals
• Gram stain: Normal flora; no predominant organisms
• AFB smear: Negative

Chest X-ray (PA view)

• Bilateral hyperinflation
• Flattening of bilateral diaphragms
• Increased AP diameter (barrel chest)
• Horizontal ribs with widened intercostal spaces
• No consolidation, collapse, or pleural effusion
• Heart size: Normal (no cardiomegaly)

Pulmonary Function Tests (Spirometry)

Total IgE

• Serum Total IgE: 480 IU/mL (markedly elevated; normal <100 IU/mL)

Skin Prick Test / RAST (Specific IgE)

• House dust mite sensitization likely

SEVERITY ASSESSMENT

DIAGNOSIS

• Occupational allergen exposure (textile dust)
• Irregular compliance with controller medication
• Lower socioeconomic status

DIFFERENTIAL DIAGNOSES

1. Acute exacerbation of COPD - ruled out by younger age, reversible obstruction, eosinophilia, elevated IgE, no significant smoking history currently, no chronic productive cough
2. Cardiac asthma (acute pulmonary edema) - ruled out by no cardiac history, no basal crackles, no cardiomegaly, no elevated JVP
3. Foreign body aspiration - ruled out by bilateral wheeze, history of known asthma, no sudden onset in previously well patient
4. Pulmonary embolism - ruled out by no pleuritic chest pain, no hemoptysis, bilateral wheeze
5. Anaphylaxis - ruled out by no allergen exposure event, no urticaria/angioedema

MANAGEMENT

Immediate (Emergency Department)

1. Posture: Sit upright; reassure patient; avoid unnecessary distress
2. Oxygen: High-flow oxygen via face mask to maintain SpO2 94-98% (target)
3. Short-Acting Beta-2 Agonist (SABA):
   • Salbutamol (albuterol) 2.5-5 mg via oxygen-driven nebulizer every 20 minutes for first hour (back-to-back nebulizations)
   • Or: Salbutamol MDI 4-8 puffs via spacer every 20 minutes
4. Short-Acting Anticholinergic:
   • Ipratropium bromide 0.5 mg nebulized with salbutamol (combined nebulization) - adds additional bronchodilation in severe attacks
5. Systemic Corticosteroids: (cornerstone of treatment)
   • Hydrocortisone 200 mg IV stat (or prednisolone 40-50 mg orally if patient can swallow)
   • Reduces airway inflammation; takes 4-6 hours for maximum effect
6. IV Access: Establish; send bloods; correct dehydration with IV fluids
7. Monitor: Continuous SpO2, cardiac monitoring, repeat PEFR/ABG at 1 hour
8. Magnesium Sulfate: 2 g IV infusion over 20 minutes (if inadequate response to initial bronchodilators - evidence-based for severe attacks)
9. Withhold: Sedatives, opiates, antihistamines (can cause respiratory depression)

If No Improvement / Worsening (ICU Admission Criteria):

• PaCO2 rising, SpO2 falling despite O2, drowsiness, silent chest
• Consider: Heliox (helium-oxygen mixture), IV salbutamol, IV aminophylline (use with caution; narrow therapeutic window)
• Prepare for non-invasive ventilation (BiPAP) as a bridge
• Intubation and mechanical ventilation as last resort (high risk of barotrauma)

After Stabilization (Ward)

• Nebulized salbutamol every 4-6 hours, then step down to MDI
• Oral prednisolone 40 mg OD for 5-7 days (no taper needed for short courses)
• Resume inhaled corticosteroid (budesonide 400 mcg BD)
• Sputum culture if secondary bacterial infection suspected
• Spirometry once stable

Discharge Planning and Long-Term Management

1. Controller therapy: Inhaled corticosteroid (budesonide) + LABA (formoterol) as per GINA step-up therapy
2. Rescue inhaler: Salbutamol MDI with spacer
3. Asthma action plan: Written plan - green/yellow/red zones based on PEFR and symptoms
4. Trigger avoidance: Occupational dust exposure counseling; N95 mask at work; allergen-proof bed covers
5. Influenza and pneumococcal vaccination
6. Compliance counseling: Importance of regular ICS use even when well
7. Spirometry follow-up in 4-6 weeks
8. Referral: Pulmonologist / Allergy specialist
9. RAST testing / Skin prick test: For specific allergen identification
10. Socioeconomic: Subsidized medication scheme enrollment

PROGNOSIS

• Immediate: Guarded but good with prompt treatment
• Long-term: Good if adherence to controller therapy is maintained, trigger avoidance practiced, and regular follow-up maintained
• Risk factors for death (present in this patient): SpO2 <90%, PaCO2 normalization, multiple prior ED visits - requires close monitoring and patient education

SUMMARY

Case History: Peptic Ulcer Disease (Duodenal Ulcer)

PATIENT DETAILS

CHIEF COMPLAINTS

1. Recurrent epigastric pain - 6 months
2. Nocturnal awakening due to pain - 3 months
3. Heartburn and acid regurgitation - 4 months
4. Nausea - occasional, 3 months
5. Black tarry stools (melena) - 2 days
6. Dizziness and generalized weakness - 1 day

HISTORY OF PRESENT ILLNESS

PAST HISTORY

• No prior diagnosis of peptic ulcer disease (first presentation to hospital)
• Migraine: Managed with aspirin 75 mg daily for 10 years + ibuprofen 400 mg as needed during attacks (significant NSAID use)
• No history of: Diabetes mellitus, hypertension, tuberculosis, cardiac disease, renal disease, liver disease, prior abdominal surgery
• No prior endoscopy
• No known drug allergies

TREATMENT HISTORY

• Aspirin 75 mg OD (daily, 10 years) - for migraine prophylaxis
• Ibuprofen 400 mg SOS (intermittent, as needed for headache)
• OTC antacids (Gelusil/Digene) - self-medication, escalating use over 3 months
• No prior PPI or H2 blocker use
• No prior H. pylori testing or treatment

PERSONAL HISTORY

• Diet: Mixed; irregular meal timings; frequent skipping of breakfast; heavy dinner late at night
• Appetite: Reduced over past 2 months (fear of pain after eating - "sitophobia" - more typical of gastric ulcer, but present here due to heartburn)
• Sleep: Disturbed (nocturnal pain)
• Bowel habits: Black tarry stools x 2 days; normally regular
• Bladder habits: Normal
• Smoking: Yes - 20 cigarettes/day for 15 years (significant; smoking delays ulcer healing and increases recurrence)
• Alcohol: Moderate (2-3 drinks/week; alcohol stimulates gastric acid secretion)
• Occupation: High-stress sedentary job; irregular meals; excessive coffee consumption (3-4 cups/day; caffeine stimulates acid secretion)

FAMILY HISTORY

• Father: History of "stomach ulcer" in the past (positive family history - genetic predisposition to hyperacidity)
• Mother: No significant illness
• No family history of gastric cancer, H. pylori-related disease, or inflammatory bowel disease

SOCIOECONOMIC HISTORY

• Upper-middle socioeconomic class
• Nuclear family; independent house
• Regular income; health insurance available
• Irregular meals, frequent eating out, high-stress urban lifestyle

GENERAL PHYSICAL EXAMINATION

SYSTEMIC EXAMINATION

Abdomen

• Abdomen flat, moves with respiration
• No visible peristalsis
• No visible dilated veins, scars, or pulsations
• Umbilicus: Centrally placed, normal
• No visible mass

• Abdomen soft
• Tenderness: Localized, moderate tenderness in the epigastric region (midline, above the umbilicus)
• No guarding, no rigidity (important - rules out perforation)
• No rebound tenderness (rules out peritonitis)
• No palpable mass
• Liver and spleen: Not palpable

• Deep epigastric tenderness - the only consistent positive finding on physical examination in uncomplicated PUD
• No succussion splash (rules out gastric outlet obstruction)
• No hepatosplenomegaly

• Tympanitic throughout
• Liver dullness: Present (rules out free gas under diaphragm / perforation)
• No shifting dullness

• Bowel sounds: Present, slightly hyperactive (active GI bleed)
• No bruit

Rectal Examination (Digital)

• Anal tone normal
• Black tarry material on examining finger (melena confirmed)
• No fresh blood, no mass, no tenderness

Cardiovascular System

• S1, S2 heard; no murmurs
• JVP: Not elevated
• Peripheral pulses: Present bilaterally, mildly weak

Respiratory System

• Normal vesicular breath sounds bilaterally
• No added sounds

Central Nervous System

• Conscious, alert, oriented
• No focal neurological deficit
• Mild dizziness (secondary to blood loss)

INVESTIGATIONS

Bedside / Urgent

Hematological Investigations

Biochemistry

Urea Breath Test (UBT) / H. pylori Tests

Radiological Investigations

• No free gas under diaphragm (rules out perforation)
• No signs of intestinal obstruction
• Normal cardiac and diaphragmatic contours

• Thickened duodenal wall in D1
• No free fluid in abdomen
• Liver, gallbladder, pancreas, kidneys, spleen: Normal
• No lymphadenopathy

Upper GI Endoscopy (OGD Scopy) - Definitive Investigation

• Esophagus: Normal
• Gastroesophageal junction: Intact; no varices; no hiatus hernia
• Stomach: Mild antral gastritis; hyperemic mucosa; no gastric ulcer
• Duodenum (D1/D2 junction - anterior wall):
  • Single, well-defined, punched-out ulcer, 12 mm x 10 mm
  • Oval shape with clean base; indurated, erythematous margins
  • Oozing vessel at ulcer base (Forrest Class IIa - visible non-bleeding vessel - high risk of re-bleeding)
  • No malignant features

• Rapid urease test (CLO test): Positive - confirms H. pylori infection
• Histology: Chronic active gastritis with H. pylori organisms (Warthin-Starry staining); no dysplasia, no malignancy

• Injection therapy with 1:10,000 epinephrine solution around the bleeding vessel
• Hemostasis achieved (no active bleeding at end of procedure)

Gastric Acid Secretory Studies (Optional)

• Serum fasting gastrin: 68 pg/mL (normal <100 pg/mL)
• Zollinger-Ellison syndrome: Excluded

SEVERITY ASSESSMENT OF UPPER GI BLEED (Rockall Score)

DIAGNOSIS

1. H. pylori gastritis (CLO test and stool antigen positive) - primary cause
2. Chronic NSAID use (aspirin + ibuprofen) - major contributing/perpetuating factor
3. Cigarette smoking - delays healing; increases recurrence
4. Lifestyle factors: Stress, irregular meals, excessive coffee, alcohol

DIFFERENTIAL DIAGNOSES

MANAGEMENT

Acute/Emergency Management (In-Patient)

• IV access x2 large-bore cannulae
• IV fluids: Normal saline / Ringer's lactate to correct hypovolemia
• Blood grouping and cross-matching; arrange 2 units packed red blood cells (PRBC) transfusion (Hb <9 g/dL + active bleed)
• Strict NPO (nil per oral)
• Continuous monitoring: Pulse, BP (postural), SpO2, urine output

• Pantoprazole/Omeprazole 80 mg IV bolus, followed by 8 mg/hour continuous infusion x 72 hours
• After 72 hours: Switch to oral PPI (Pantoprazole 40 mg BD)
• IV PPI raises gastric pH >6, stabilizing the clot at the ulcer base and preventing re-bleeding

• Epinephrine injection + thermal/mechanical therapy as needed
• Repeat endoscopy at 24 hours if re-bleeding suspected

• Transfuse packed red blood cells to maintain Hb >8 g/dL (restrictive transfusion strategy in hemodynamically stable patients)
• Fresh frozen plasma only if coagulopathy

• Stop aspirin and ibuprofen immediately
• Discuss alternative migraine management (e.g., sumatriptan, preventive therapy) with neurology

• Eradication reduces 1-year ulcer recurrence from ~75% (PPI alone) to <10%

After Stabilization (Ward Continuation)

• Oral PPI (Pantoprazole 40 mg OD) for 4-8 weeks post-H. pylori eradication
• Iron supplementation: Ferrous sulfate 200 mg TDS for iron deficiency anemia
• Soft, bland diet; small, frequent meals; avoid spicy food, coffee, alcohol
• Dietary counseling: Avoid long fasting intervals; no late-night meals
• Continue PPI during active bleed recovery; maintain for 6-8 weeks total

Monitoring

• Repeat Hb after 48 hours; watch for re-bleed
• Signs of re-bleed: Fresh hematemesis, hematochezia, drop in Hb, tachycardia, hypotension
• Repeat endoscopy if re-bleed suspected (second endoscopy in Forrest IIa)

FOLLOW-UP AND LONG-TERM MANAGEMENT

1. Confirm H. pylori eradication:
   • UBT or stool antigen 4-8 weeks after completing eradication therapy and stopping PPI for 2 weeks (PPI suppresses H. pylori and can give false negatives)
   • Do NOT use serum IgG for confirming eradication
2. Repeat OGD scopy in 6-8 weeks (mandatory for duodenal ulcer with bleeding - to confirm healing and exclude malignancy)
3. Long-term PPI maintenance: Only if:
   • H. pylori eradication fails
   • NSAID use must be continued (give PPI cover)
   • High-risk patients (elderly, prior ulcer complications)
4. NSAID/Aspirin guidance:
   • Avoid regular NSAID use
   • If low-dose aspirin must be resumed (e.g., cardiovascular indication), use with PPI cover
   • Prefer selective COX-2 inhibitors if anti-inflammatory therapy unavoidable
5. Lifestyle modification:
   • Stop smoking (smoking delays healing and increases recurrence risk)
   • Reduce alcohol intake
   • Regulate meal timings; avoid excessive coffee
   • Stress management counseling
6. Alarm symptoms requiring urgent re-evaluation:
   • Recurrent hematemesis or melena
   • Progressive weight loss
   • Dysphagia or early satiety (suggests gastric outlet obstruction)
   • New-onset anemia

COMPLICATIONS OF PUD (To Counsel Patient)

PROGNOSIS

• Immediate: Good with prompt endoscopic + medical management; re-bleed risk ~25% at 72 hours (Forrest IIa)
• Long-term: Excellent with successful H. pylori eradication (<10% recurrence at 1 year)
• If NSAID use continues without PPI cover: Poor; high risk of recurrent ulcer and re-bleeding
• If smoking continues: Delayed healing; increased recurrence

SUMMARY