EMERGENCY: Altered Level of Consciousness After Severe Vomiting

Step 1 - Immediate Actions (First 5 Minutes)

Step 2 - Differential Diagnosis

1. Severe Dehydration + Electrolyte Disturbance (Most Likely)

• Hyponatremia - loss of Na+ in vomitus + replacement with hypotonic fluids OR no intake. Acute hyponatremic encephalopathy causes cerebral edema and progresses to seizures, brainstem herniation, coma, and death. As Harrison's states: "Acute hyponatremic encephalopathy ensues when volume regulatory mechanisms are overwhelmed by a rapid decrease in tonicity, resulting in acute cerebral edema."
• Hypokalemia - severe K+ loss from vomiting
• Metabolic alkalosis - from H+ loss in gastric contents
• Hypoglycemia - no intake + repeated vomiting

2. Wernicke Encephalopathy (Thiamine Deficiency)

3. Medication Toxicity / Overdose

4. Aspiration + Hypoxia

5. Cerebral Event (must exclude)

6. Addisonian Crisis (Adrenal Insufficiency)

Step 3 - Immediate Investigations

Step 4 - Treatment

Empirical Treatment (Do Not Delay for Results)

• Acute hyponatremia (symptomatic, comatose): 3% hypertonic saline - target raise Na+ by 1-2 mEq/L/hour for the first few hours (to stop cerebral edema) - but do not correct >8-10 mEq/L in first 24 hours (risk of osmotic demyelination)
• As Tintinalli's states: "When the patient presents with severe neurologic symptoms (vomiting, seizures, reduced consciousness), the most important guide for therapy is symptoms rather than the serum Na+"

Step 5 - Warning Signs That Change Management

Summary

• This patient needs emergency care NOW - he cannot protect his airway
• The most likely cause is acute electrolyte disturbance (hyponatremia/hypokalemia) from prolonged vomiting
• Wernicke encephalopathy must be treated empirically - give thiamine BEFORE glucose
• Do NOT give hypotonic IV fluids
• Check blood glucose at bedside within the first minute
• Consider intubation if GCS does not improve rapidly

• Harrison's Principles of Internal Medicine 22E (2025) - Hyponatremia, p. 2757-2764
• Goldman-Cecil Medicine - Wernicke Encephalopathy, p. 3586-3652
• Tintinalli's Emergency Medicine - Treatment of Electrolyte Disorders

Paracetamol (Acetaminophen) Dose for a 17 kg Child

Dose Calculation

Volume to Give

Dosing Schedule

Practical Prescription

Paracetamol syrup 250 mg/5 mL Give 5 mL (250 mg) orally every 4-6 hours as needed for fever/pain. Do not exceed 5 doses in 24 hours.

• Do not give more frequently than every 4 hours
• Do not combine with other paracetamol-containing products (cold syrups, etc.)
• If fever persists >3 days or is >40°C, seek medical review

CT scan: Top-of-basilar syndrome showing bilateral medial thalamic infarcts and right occipital infarct - Neuroanatomy through Clinical Cases, 3rd Ed.

Bilateral Cerebral Hemisphere Infarcts + Severe Basilar Artery Narrowing - Causes

Understanding the Anatomy First

• Posterior cerebral arteries (PCAs) - supplying medial temporal and occipital lobes
• Thalamo-perforating arteries - bilateral thalamic supply
• Superior cerebellar arteries
• Pontine perforators

Causes - Classified by Mechanism

1. Intracranial Atherosclerosis (Most Common Overall)

• In-situ thrombosis on the plaque surface
• Artery-to-artery embolism - plaque ruptures and debris embolizes distally to bilateral PCAs
• Branch occlusion - plaque blocks origins of perforating arteries

2. Cardioembolism

3. "Top-of-Basilar" Syndrome

• Bilateral occipital lobe infarcts (cortical blindness)
• Bilateral thalamic infarcts (altered consciousness, memory loss)
• Midbrain infarcts (somnolence, diplopia, abnormal pupils)
• The basilar artery itself may appear narrowed from the embolus or underlying atherosclerosis

4. Vertebral Artery Dissection

5. Vasculitis - Inflammatory/Autoimmune

6. Hypercoagulable States

• Antiphospholipid syndrome - recurrent strokes in young patients; anti-cardiolipin antibodies
• Polycythemia vera - hyperviscosity
• Essential thrombocythemia
• Protein C / Protein S / Antithrombin III deficiency
• Factor V Leiden mutation
• Nephrotic syndrome (hypercoagulable from loss of anticoagulant proteins)
• Malignancy (Trousseau syndrome) - mucin-secreting adenocarcinomas

7. Basilar Artery Dolichoectasia

8. Hemodynamic (Watershed) Infarction

9. Genetic / Metabolic Causes (Rare)

• MELAS (mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes) - stroke-like episodes NOT in vascular territory; bilateral; associated with seizures, lactic acidosis
• CADASIL (cerebral autosomal dominant arteriopathy) - young adults, leukoencephalopathy
• Fabry disease - alpha-galactosidase A deficiency; preferentially affects posterior circulation

Key Investigative Approach

Summary

Can Wernicke Encephalopathy or Severe Dehydration from Vomiting Cause Bilateral Cerebral Infarcts + Basilar Artery Narrowing?

1. Wernicke Encephalopathy (WE)

Can it directly cause cerebral infarcts? - NO (not true arterial infarcts)

Can it mimic infarcts on imaging? - YES, powerfully

Thiamine is an essential cofactor for energy metabolism. Its deficiency causes selective failure of oxidative metabolism in high-demand brain regions - not arterial occlusion.

The critical imaging trap:

• WE causes bilateral medial thalamic signal changes on MRI that look exactly like bilateral thalamic infarcts
• The DWI restriction (bright on diffusion-weighted imaging) mimics acute ischemic infarct
• This is the same pattern as "top-of-basilar" syndrome (bilateral thalamic + occipital infarcts from basilar apex occlusion)
• It is very easy to misdiagnose WE as bilateral PCA territory infarction

Does WE cause basilar artery narrowing? - NO

• A coincidence (the stenosis is the actual cause of thalamic infarcts)
• Artefact on MRA from slow/turbulent flow rather than true stenosis

WE can be caused by vomiting - YES

• Hyperemesis gravidarum
• Malignant GI obstruction
• Prolonged vomiting from any cause (including our motion sickness patient)

2. Severe Dehydration from Vomiting

Can it cause bilateral cerebral infarcts? - YES, via several mechanisms

A. Cerebral Venous Sinus Thrombosis (CVST) - Most important mechanism

"Most often, this (venous sinus thrombosis) occurs during a hypercoagulable state related either to dehydration, infection, or childbirth."

• Bilateral thalamic venous infarcts (can look like bilateral deep infarcts)
• Altered consciousness progressing to coma
• Nausea and vomiting (both a cause and symptom)

B. Hemodynamic/Watershed Infarction

C. Hyponatremia-induced Cerebral Edema (not infarction, but mimics it)

Can dehydration narrow the basilar artery? - INDIRECTLY

• Hemoconcentration + hypotension in the setting of pre-existing atherosclerotic plaque can trigger in-situ thrombosis on a narrowed basilar artery, making it appear severely stenosed on imaging
• MRA performed during dehydration/hypotension may show apparent "narrowing" due to slow or reduced flow rather than true stenosis (flow-related artifact)

3. The Combined Picture - Putting It Together

Severe Vomiting
     │
     ├── Thiamine depletion → WERNICKE ENCEPHALOPATHY
     │        └── Bilateral thalamic metabolic necrosis
     │            (mimics bilateral thalamic infarcts on MRI)
     │
     ├── Dehydration → CVST
     │        └── Bilateral thalamic venous infarcts
     │            (especially with deep venous thrombosis)
     │
     ├── Hypovolemia + pre-existing basilar stenosis
     │        └── Hemodynamic infarcts in posterior territory
     │
     └── Hyponatremia
              └── Cerebral edema → secondary ischemia

Clinical Bottom Line

Most important clinical action: