6 Oct 2025

The Burning Within: A Fight for Life After Acid Ingestion

1) Diagnosis

  • Primary Diagnosis: Severe corrosive gastric injury (acid poisoning) with fundic necrosis and probable gastric perforation.
  • Secondary / Complicating Conditions:
    • Hypovolemic + distributive shock
    • Severe metabolic acidosis
    • Acute kidney injury (oliguria)
    • Severe anemia (Hb 3.1 g/dL)
    • Generalized anasarca and pleural effusion
    • Post-acid ingestion status s/p Jejunostomy (Day 3)

2) History of Present Illness (HPI)

18-year-old female was brought to the ER after intentional acid ingestion (unknown quantity). She was unconscious, unresponsive, with rapid breathing, weak pulse, and cold extremities. There was no history of trauma, fever, or seizure before ingestion. No hematemesis reported by relatives, but acid smell noted around the mouth.
Negative history: No diabetes, hypertension, or drug overdose.

3) Past Medical History

  • No known chronic illness (HTN/DM/CAD/CKD).
  • No previous surgeries or ICU admissions.
  • No drug allergies or regular medications.

4) Physical Examination

  • General: Pale, cold, clammy; unresponsive (GCS E1 Vt M1); severe distress.
  • CVS: Tachycardic, weak thready pulse, severe hypotension.
  • RS: Tachypneic, clear initially; bilateral basal crepts later due to effusion.
  • CNS: Unresponsive but pupils equal/reactive.
  • Abdomen: Tender, rigid later; distension developed on Day 2.
  • Extremities: Cold peripheries, mild edema by Day 2.

5) Vitals on Admission

  • HR 138 bpm
  • BP 60/30 mmHg
  • RR 38/min
  • Temp 98.4 °F
  • SpO₂ 86% on room air
  • GCS E1 Vt M1

6) Echocardiography (ECHO)

  • LV normal size, EF ~ 55%.
  • No RWMA.
  • Valves normal.
  • No pericardial effusion.
    • Shock likely non-cardiogenic (distributive/hypovolemic).

7) Investigations

TestResultInterpretation
Hb 3.1 g/dL Severe anemia, probable GI bleed
WBC 12 000/mm³ Stress leukocytosis
Platelets 200 000/mm³Normal
Urea/Cr 70/2.1 mg/dL AKI (pre-renal)
Na/K140/3.4 mEq/L Mild hypokalemia
LFT Normal —
ABG pH 6.95, HCO₃ 7 Severe metabolic acidosis
INR1.8Coagulopathy
Lactate6.5 mmol/L Poor perfusion

Follow-up Trends:

Day Na K Cr ABG(pH)Lactate
01403.42.16.956.5
11423.72.07.154.2
31384.01.67.302.8

8) Imaging

  • CT Abdomen (5 Oct 2025, Universal Hospital)
  • Ill-defined, sloughed stomach wall, mainly fundus → perforation suspected.
  • Pneumoperitoneum, severe ascites, mesenteric haziness.
  • Long-segment edema in proximal small bowel + mild colonic wall thickening.
  • Moderate bilateral pleural effusion with basal collapse.
  • Generalized anasarca.

Impression: Severe corrosive gastritis with fundic necrosis ± perforation.

9) ECG & RBS

  • ECG: Sinus tachycardia, no ischemic changes.
  • RBS: 110 mg/dL.

10) Day by Day Management

  • Day 0 – Emergency Admission to ICU
    • Presentation: Unconscious, unresponsive, shallow breathing, hypotension (BP 60/30 mmHg), HR 146/min, RR 36/min, SpO₂ 82% RA, Temp 99°F, GCS E1 Vt M1
    • ABG: pH 6.98 / HCO₃⁻ 8 / pCO₂ 24 / PaO₂ 72 → Severe metabolic acidosis
    • Hb 3.1 g/dL, Lactate > 6 mmol/L
  1. Airway & Ventilation
    • Emergency intubation (ET 7.0 fixed at 20 cm)
    • Mechanical ventilation: SIMV mode, FiO₂ 100%, TV 6 mL/kg, PEEP 5 cm H₂O
    • Sedation: Midazolam 2 mg/h + Fentanyl 50 µg/h (for ventilator synchrony and pain control)
  2. Circulation
    • 2 wide-bore IV lines + central line (RIJ)
    • Crystalloid bolus 2 L NS, followed by maintenance 200 mL/h
    • Norepinephrine 0.2 µg/kg/min, titrated to MAP > 65 mmHg
    • Vasopressin 0.03 U/min adjunct
    • 4 units PCV + 6 units FFP transfused → target Hb > 8 g/dL
  3. Investigations ordered
    • CBC, RFT, LFT, Coagulation profile, ABG every 4 h, Trop-I, Serum electrolytes, ECG, Urine output monitoring.
    • Output: Urine 5 mL/h → Oliguria due to shock & renal hypoperfusion → Added Furosemide 40 mg IV stat, poor response → continued fluid and vasopressors.
  4. Medications initiated
DrugDoseRationale
IV Ceftriaxone2 g OD Broad spectrum coverage
Pantoprazole 200 mg IV infusion@4ml/hr Stress ulcer prophylaxis / acid control
Ondansetron4 mg IV TDS Prevent retching / aspiration
NaHCO₃20 mEq IV slow × 2 then infusionSevere metabolic acidosis
Mucomix (N-acetylcysteine) infusion Mucolytic & antioxidant effect on GI mucosa
Inj Tranexamic acid500 mg TDS For upper GI mucosal bleeding risk
  • Day 1
    • Vitals: BP 82/50 (MAP 62), HR 128, RR 24 (ventilated), SpO₂ 94% on FiO₂ 60%
    • Urine Output: 15 mL/h
    • ABG: pH 7.12, HCO₃⁻ 12, Lactate 4.2 mmol/L (Improving)
    • Hb 8.1 g/dL, Cr 1.8 mg/dL
    • Changes / Additions
      • Continued noradrenaline 0.18 µg/kg/min, vasopressin 0.02 U/min
      • NaHCO₃ infusion slowed as pH > 7.1
      • IV Metronidazole 500 mg TDS added → anaerobic coverage
      • IV Albumin 20% 100 mL OD for hypoproteinemia and oncotic support
      • Urine output target > 0.5 mL/kg/h — started low-dose dopamine 2 µg/kg/min for renal perfusion
    • Investigations:
TestDay 0Day 1
Hb (g/dL) 3.1 8.1
WBC (/mm³)1100014200
Plt (/mm³)190000165000
Cr (mg/dL)1.2 1.8
Na⁺ (mEq/L)138134
K⁺ (mEq/L) 4.2 4.8
Lactate (mmol/L) >6 4.2
  • Day 2
    • Vitals: BP 98/60, HR 110, SpO₂ 96% FiO₂ 40%, Temp 99.5°F
    • Urine output: 30 mL/h (Improving)
    • ABG: pH 7.28 / HCO₃⁻ 18 / pCO₂ 32
    • Labs: Cr 1.5 mg/dL, WBC 15 000
    • CT Abdomen (Plain – Reported 5 Oct 2025):
      • Stomach wall ill-defined and sloughed off (mainly fundus & greater curvature) → suggestive of perforation / gangrenous gastritis
      • Severe ascites with pneumo-peritoneum
      • Left > Right pleural effusion with basal collapse
      • Long segment edematous small bowel wall thickening, mild colonic thickening, generalized anasarca
    • Interpretation:
      • Severe corrosive gastric necrosis with perforation and peritonitis → Surgical intervention required.
    • Plan:
      • Continue ventilatory and vasopressor support
      • Start Meropenem 1 g TDS IV + Fluconazole 100 mg IV OD (antifungal coverage)
      • Shift for surgical exploration and Jejunostomy planning once hemodynamically stable.
      • NPO, Ryle’s tube for drainage, monitor gastric aspirate.
  • Day 3 – Jejunostomy Surgery
    • Pre-op:
      • Patient on FiO₂ 40%, PEEP 5, MAP > 65 on norad 0.12 µg/kg/min
      • Urine output adequate, lactate 3 mmol/L
      • Surgery consent taken, high-risk explained
    • Intra-op Findings:
      • Extensive necrosis of stomach wall with slough and perforation at fundus/body junction.
      • Peritoneal soiling with acidic fluid.
      • Jejunostomy feeding tube placed (distal jejunum) + peritoneal lavage.
      • Nasogastric tube left in situ for drainage.
    • Post-op ICU Management:
      • Ventilatory support continued SIMV FiO₂ 40%
      • Sedation: Midazolam 1 mg/h + Fentanyl 40 µg/h
      • Antibiotics: Meropenem + Fluconazole continued
      • Vasopressors weaned over next 12 h
      • Enteral feeding via Jejunostomy started @ 10 mL/h after 24 h
      • ABG: pH 7.36 / HCO₃⁻ 21 / Lactate 2.4 → near normalization
  • Day 4–5 (Recovery Phase)
    • Extubated to O₂ via HFNC FiO₂ 35%
    • Norad off > 24 h
    • Jejunostomy feeds advanced to 30 mL/h
    • Urine output maintained > 0.7 mL/kg/h
    • CRP down from 188 → 72 mg/L
    • Hematocrit stable, Renal function normalized

11) Pathophysiology (Specific to Acid Poisoning with Shock and Gastric Necrosis)

  • Mechanism of Acid Injury
    • Corrosive acids (e.g., hydrochloric, sulfuric, nitric) have low pH (<2) and cause coagulative necrosis.
    • The hydrogen ions denature proteins, precipitate structural proteins, and create an eschar (coagulum) that may initially limit deeper penetration.
    • However, in high concentrations, continued proton diffusion and heat generation lead to deep transmural necrosis and perforation, especially in the stomach.
  • GI Tract Injury Pattern
SiteMechanismResult
Oropharynx & EsophagusRapid contact, superficial burns (if swallowed quickly)Odynophagia, dysphagia
Stomach (Fundus & Body)Pooling of acid → prolonged contact + high concentrationTransmural necrosis, perforation, and hemorrhage
Small Intestine (Proximal loops)Secondary injury from acid spill during vomiting or perforationEdematous wall thickening and serositis (as seen on CT)
  • Systemic Absorption and Metabolic Effects
    1. Metabolic Acidosis
      • Caused by systemic absorption of hydrogen ions and tissue hypoperfusion.
      • In this case, ABG pH 6.98, HCO₃⁻ 8 mEq/L, Lactate > 6 mmol/L, confirming combined metabolic acidosis (acid load + lactic acidosis from shock).
    2. Hemorrhagic Shock
      • Massive mucosal bleeding from gastric necrosis → Hb 3.1 g/dL.
      • Severe hypovolemia → ↓ preload → ↓ cardiac output → hypotension (60/30 mmHg) → catecholamine surge, tissue hypoxia, further lactic acid accumulation.
    3. Distributive Component (Toxic Shock)
      Inflammatory cytokines (TNF-α, IL-1β, IL-6) released from necrotic tissue → vasodilation + capillary leak → generalized anasarca, as seen on CT.
    4. Renal Hypoperfusion → AKI
      • Hypotension and myoglobin/heme pigment load → acute tubular necrosis.
      • Manifested as oliguria (5 mL/h) and ↑creatinine (1.8 mg/dL on Day 1).
  • Local to Systemic Transition
Stage Local Pathology Systemic Response
Stage 1 (Chemical Burn) Coagulative necrosis of mucosa, eschar formationNausea, hematemesis, pain
Stage 2 (Tissue Penetration) Sloughing, vascular thrombosis, perforationSepsis, peritonitis
Stage 3 (Systemic Decompensation)Bacteremia, cytokine storm SIRS → MODS → Shock
Stage 4 (Repair/Stricture) Fibrosis during healing Gastric outlet obstruct
  • Why This Patient Deteriorated Rapidly
    • Large-volume acid ingestion → deeper gastric burn → rapid perforation and hemoperitoneum.
    • Delayed gastric emptying worsened contact time at the fundus and greater curvature.
    • Massive GI bleed dropped Hb → hypoxia-driven lactic acidosis.
    • Severe metabolic acidosis reduced cardiac contractility, amplifying hypotension.
    • Cytokine storm + vasoplegia made shock refractory → need for noradrenaline + vasopressin.
  • Rationale for Jejunostomy
    • After gastric perforation, enteral nutrition via stomach becomes impossible.
    • Jejunostomy bypasses injured stomach, providing early enteral feeding, preventing catabolic state, improving gut barrier integrity, and reducing infection risk.
    • It also allows the stomach to remain NPO for healing and drainage.
  • Sequential Organ Impact in This Case
Organ/System Pathophysiologic Mechanism Clinical/Lab Evidence
Gastrointestinal Acid-induced coagulative necrosis → perforationCT: gastric sloughing, pneumoperitoneum
Cardiovascular Hypovolemia + vasoplegia→ shockBP 60/30, tachycardia
Renal Ischemic ATN from shock Oliguria, Cr ↑ to 1.8 mg/dL
Respiratory Aspiration + pleural effusion CT: mild–mod effusions
Hematologic Massive upper GI bleed Hb 3.1 → 4 PCV + 6 FFP transfused
MetabolicLactic + hydrogen ion acidosis pH 6.98, HCO₃⁻ 8, Lactate > 6

12) Discharge Medicines (once stabilized, post-ICU)

  • Pantoprazole 40 mg OD – acid suppression.
  • Sucralfate syrup TDS – mucosal protection.
  • Ceftriaxone 1 g IV BD (5 days) – infection prophylaxis.
  • Ranitidine via FJ (step-down).
  • Multivitamins + Protein supplement (via FJ).

13) Key Notes / Clinical Pearls

  1. Always secure airway early in corrosive ingestion.
  2. Avoid gastric lavage or induced vomiting → re-exposure risk.
  3. CT Abdomen (plain) is diagnostic for necrosis/perforation.
  4. Jejunostomy feeding allows nutrition while bypassing damaged stomach.
  5. Acidosis correction + hemodynamic stability are vital for surgical timing.

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