Drowning

Case contributed by Yaïr Glick
Diagnosis certain

Presentation

Drowned in the sea.

Patient Data

Age: 20 years
Gender: Male

Mobile x ray at the shock room

x-ray

Properly placed ventilation tube. Coarse bilateral perihilar nodulointerstitial opacities.

CT head, immediately after

ct

NGT though right nostril, ventilation tube through mouth.
CSF spaced preserved, gray-white matter interface preserved.
Air-fluid levels in all paranasal sinuses, most probably representing sea water.
Nasopharyngeal and oropharyngeal edema, probably due to instrumentation.

CT chest with CT head

ct

Widespread ground glass opacities over both lungs. Numerous small patchy alveolar opacities in all lung lobes. Dependent consolidations in lower lobes.

Chest x ray 1 day later

x-ray

Subclavian line on right, its tip projected over the SVC. Mild interstitial thickening - considerable improvement.

CT head 2 days later

ct

Diffuse cerebral and cerebellar edema with sulcal and cisternal effacement. The third ventricle is effaced. The falx cerebri and tentorium cerebelli are prominent due to diffuse edema - pseudo-subarachnoid hemorrhage. Biparietal scalp edema.

CT chest

ct

Only the dependent consolidations have remained.

Chest x ray 3 days later

x-ray

There is a large opacity in the right hemithorax. The mediastinum and the heart are pulled to the right. Most probably collapse of both right lower lobe and right middle lobe.
Prominent interstitial perihilar markings in left lung.

CXR 1 day later after...

x-ray

CXR 1 day later after respiratory physioRx

Beside the properly placed double-lumen right subclavian line, there is a right jugular single-lumen line that ends adjacent to the 2nd rib.

Bilateral interstitial edema but the right lung atelectasis has cleared.

CT head 1 day later

ct

Diffuse cerebral and cerebellar edema, unchanged.
After injecting IV contrast material, the intracranial arteries do not opacify.

Case Discussion

Young male, history remarkable for thalassemia minor and heavy smoking. The lifeguard reported that the patient had been submerged for about 3 minutes. Pulled out of the water unconscious, not breathing and pulseless. Received prompt CPR on the spot for 10 minutes till return of pulse. Ventilated on the spot. Taken to nearby hospital. At the ER: unconscious, tachycardic, ventilated, pupils unresponsive to light, recurring seizures. Very severe metabolic and respiratory acidosis: pH 6.58, pCO2 92 mmHg, base excess -26 mmol/L, bicarbonate 3.8 mmol/L. Treated with toxoid and transferred to the ICU in critical condition, APACHE II score of 28.

On admission to the ICU: GCS 3TS, narrow pupils unresponsive to light, no corneal reflex, no oculocephalic reflex. Received pressure-controlled ventilation (PCV) and treated with IV fluids, nutrition via NGT, ranitidine, enoxaparin (to prevent DVT), and empiric ceftriaxone. Treated for status epilepticus with midazolam, propofol, phenytoin, and even required thiopentone. The seizures stopped. Received norepinephrine for hypotension. Two days later, sedation was discontinued.

During his hospitalization at the ICU, the following problems were encountered:

  • Severe anoxic brain damage: Despite discontinuation of sedation, remained with GCS 3. Repeat CT brain 3 days after the first showed severe cerebral-cerebellar edema. Started on mannitol. EEG: no certain brain activity. Repeat CT 5 days later showed no improvement in brain edema. The intracranial arteries did not opacify at CTA. Developed diabetes insipidus, responded well to desmopressin.
  • Hemodynamic instability: Shortly after admission, required norepinephrine due to hemodynamic instability despite fluid resuscitation. Echocardiogram normal, IVC not collapsed. Pulmonary pressure moderately elevated. Due to increasing doses of vasopressors, started on steroids. Waned off vasopressors 8 days into admission.
  • Acute lung injury (ALI): Developed ALI due to aspiration. Following intensive treatment, the clinical and radiological picture of ALI vanished.
  • RLL atelectasis: Deterioration in ventilatory status 6 days into admission. Chest x ray showed complete RLL atelectasis. Significant clinical and radiological improvement after receiving high PEEP and respiratory physiotherapy.
  • Acute kidney injury: Following CPR, creatinine reached 2.1 mg/dL. Following IV fluid resuscitation, blood pressure stabilization by norepinephrine and steroids and furosemide administration, urinated well. Creatinine dropped to norm.
  • Acute liver injury: On admission, significant deterioration in liver function tests, expecially transaminases - an expression of ischemic hepatitis. After stabilization, liver function tests improved vastly.

11 days into admission, there was significant deterioration in his hemodynamic state, probably due to brain herniation, and he died.

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