: ;̂ -ll 26 ^ f̂l 3 á:Vol. 26, No. 3, September, 2011 / http://dx.doi.Org/10.4266/kjccm.2011.26.3.196 Bill

Successful Recovery after Drowning byEarly Prone Ventilatory Positioning and Use of Nitric Oxide Gas

- A Case Report -

Joo Myung Lee, M.D., Jae Ho Lee, M.D., Ph.D.*,Choon-Taek Lee, M.D., Ph.D.* atid Young-Jae Cho, M.D., MPH*

Division of Cardiology, Department of Intemal Medicine, Seoul National University Hospital,Seoul National University College of Medicine, Seoul,

*Division of Pulmonary and Critical Care Medicine, Department of Intemal Medicine,Seoul National University Bundang Hospital, Seoul National University College of Medicine, Seongnam, Korea

Drowning is the third leading cause of unintentional accidental death globally. The most serious pathophysiologicconsequence of drowning is hypoxemia from acute respiratory distress syndrome. Herein, we report a drowning vic-tim who presented with hypotheniiia and cardiac arrest, followed by acute respiratory distress syndrome, rhabdo-myolysis (with acute kidney injury), and disseminated intravascular coagulopathy. Aided by advanced cardiac lifesupport and mechanical ventilation in a prone position, the patient fully recovered after two days of hospitalization.Recovery was largely attributed to early prone ventilatory positioning and use of nitric oxide gas.

Key Words: drowning, near drowning, prone position, ventilators, mechanical, nitric oxide, respiratory distress syn-drome, adult.

Drowning is the third leading cause of unintentional acci-

dental death globally.[1] The most serious pathophysiologic

consequence of drowning is hypoxemia due to acute respiratory

distress syndrome (ARDS) and resultant multiple organ failure

(M0F).[2] Previously, Coskun et al. [3] reported successful res-

cue of drowning patient with sustained extracorporeal mem-

brane oxygénation (ECMO) (about 117 days) for treatment of

ARDS. However, the ECMO has many detrimental complica-

tions including vascular complication such as bleeding, hemol-

ysis, thrombosis, distal malperfusion, which results in prono-

longed mechanical ventilation. Instead of ECMO, inhaled nitric

oxide gas could be an altemative rescue therapy for ARDS.

Nitric oxide activate soluble guanylyl cylcase, leading to the

activation of cyclic guanosine 3',5'-monophosphate (cGMP)-

Received on lune 14, 2011, Revised on August 1, 2011, Accepted onAugust 16, 2011Correspondence to: Young-Iae Cho, Division of Pulmonary and Critical

Care Medicine, Department of Intemal Medicine, SeoulNational University Bundang Hospital, Seoul NationalUniversity College of Medicine, 166 Gumi-ro, Seongnam463-707, KoreaTel: 82-17-310-0495, Fax: 82-31-787-4051E-mail: Iungdrcho@gmail.com

dependent protein ldnase (cGKI). In turn cGKI decreases the

sensitivity of myosin to calcium-induced contraction and dilate

vasctilar smooth muscle cell. [4] On the basis of this theory,

inhaled nitric oxide gas is delivered directly to areas of the

ventilated lung to improved ventOation-perfusion mismatch, re-

sulting in improved oxygénation and relieving pulmonary hy-

pertension resulting from regional hypoxia.[4,5] In addition to

itihaled nitric oxide gas, prone ventilatory positioning has been

tised as a rescue maneuver because many trials have consistentely

shown that it increases arterial oxygen tension (PaOa) in most

patients with ARDS, allowing a reduction in the fraction of

inspired oxygen (FÍO2), despite of uncertain survival benefit.[6]

Herein, we report a drowning victim who presented with hypo-

thermia and cardiac arrest, followed by ARDS with MOF. The

patient fully recovered and it was largely attributed to early

prone ventilatory positioning and use of inhaled nitric oxide

gas.

196

Joo Myung Lee, et al • Drowtdng Rescue by Prone Ventilatory Positioning 197

CASE REPORT

In April 2011, a 21-year-old Special Forces soldier drowned

while parachuting after roughly five minutes of cold river

submersion. Basic life support was initiated, and within 25 mi-

nutes, he was at a nearby military hospital - tmconscious, hy-

pothermie (30.7°C), and in cardiac arrest. Endotracheal in-

tubation and advanced cardiac life support were performed.

Cardiac rhythm resumed to sintis tachycardia after five mi-

nutes, later converting to atrial fibrillation (Fig. 1). Arterial

blood gas at FÍO2 of 1.0 returtied a pH of 6.976; PaCOi, 61.8

mmHg; PaO2, 90.8 mmHg; and SaO2, 89.3%. Acute respiratory

distress syndrome (ARDS) was subsequently diagnosed, based

on initial P/F ratio and diffuse, bilateral radiographie consoli-

dation. Despite assisted ventilation, arterial O2 saturation de-

clined to 82% with severe metabolic acidosis. As shock and

gross myoglobinuria also developed, he became anuric. At this

point, he was taken to Seoul National University Buiidang

Hospital, five minutes away. On arrival at the intetisive care

unit, his blood pressure (BP) dropped to 75/41, his body tem-

perature was 32.0°C, and arterial O2 saturation remained at

82%. Both pupils were fully dilated with sluggish light re-

fiexes and his Glasgow Coma Scale was ElVeMl. Although

trauma series x-ray showed no abnormality of cervical spine,

diffuse and bilateral consolidation showed in whole ltmg fields

(Fig. 2A). Initial laboratory findings reflected MOF, including

severe metabolic acidosis (arterial pH 7.019; bicarbonate, 15.2

mmol/L; lactic acid, 13.0 mmol/L), prothrombin time prolonga-

tion with hypofibrinogenemia (PT, 33%; INR, 2.43; fibrinogen,

59 mg/dl; and D-dimer >20 ^g/ml), acute renal failure

(creatinine, 1.33 mg/dl), ischémie hepatitis (AST/ALT, 202/195

IU/L), suspected ischémie cardiac injury (CK/CK-MB/Tnl,

589/33.5/1.59 ng/ml), and elevated serum muscle enzymes

(LDH, 1,150 IU/L; myoglobin, 1,402 ng/ml) with myoglobi-

nuria (4,000 ng/ml). Crystalloids and inotropie agents were rap-

idly infused, accompanied by active re-warming for hypothe-

rmia. Despite sodium bicarbonate push, arterial pH and HC03-

levels did not exceed 7.2 and 20.0 mmol/L, respecdvely. Since

rhabdomyolysis was likely, early continuous veno-venous hemo-

diañltration (CVVHDF) was initiated. Treatment for suspected

Die was also given (anti-thrombin III, 1,000 IU; cryoprecipitate,

44 pints). Two hours after arrival on our hospital, the patient's

BP finally normalized with inotropies and sinus tachycardia re-

stored with rapid correction of metabolic acidosis. Gradual im-

provement in mental status also occurred (with E3VeM2 in

GCS score), the myoglobinuria disappeared, and the DIC resolved.

However, hypoxemia persisted, even at high positive end ex-

piratory pressure (PEEP) with FÍO2 1.0 and inhaled nitric ox-

ide gas up to 40 ppm. Firstly, use of veno-venous ECMO was

considered, but copious post-aspiration secretions were prohi-

bitive. We instead chose to mechanically ventilate him in prone

position. Before re-positioning, neurologist rapidly examined the

patient and confirmed none of lateralizing signs with gradual

improvement of mentality. The patient was sedated, and

re-positioned to prone. Along with aggressive endotracheal suc-

tion and inhalation of nitric oxide gas, arterial saturation and

PaO2 returned to 98% and 108 mmHg, respectively within two

hours. Mixed venous oxygen saturation rose to 81.7% at five

hours, signaling reversal of hypoxemia and shock. Once vital

signs stabilized, CVVHDF was boosted to remove the excess

of fluids infused earlier. At 20 hours, the patient's ventilatory

status was noticeably better (pressure control, 22.0 cm H2O;

PEEP, 10.0 cm H2O; EÍO2 tapered to 0.6; nitric oxide gas ta-

pered/discontinued). Chest x-rays progressively improved (Fig.

2C), as did pupillary dilatation and light reflex. He was even-

Fig. 1. (A) Sinus tachycardia following CPR; later converted to atrial fibrillation with rapid ventricular response. (B) Sinus rhythm restored, twodays after admission.

198 4 2 i «1-S14 : 4 26 i l 4 3 :£ 2011

Fig. 2. (A) Initial ehest X-ray at admi-ssion to ICU. (B) After pronepositioning. (Q Slight improve-ment of bilateral eonsolidationat Day 2, after repositioning(supine). (D) Near-total elearingof bilateral consolidation atDay 5.

tually re-positioned to supine and sedation was stopped.

Twenty-one hours from admission, the patient regained mental

alertness. An extensive neurologie assessment, including brain

CT, found no evidence of hypoxie eneephalopathy. At 45

hours, respiration was stable, and eehocardiography showed

global hypokinesia but near normal ejection fraction (51%),

then extubation was done. Following short-term high-flow nasal

oxygen system support, the patient fully recovered. He was ul-

timately discharged, asymptomatic and complication-free, five

days after admission.

[ DISCUSSION

An estimated 376,000 people drowned worldwide in 2002.[1]

The most serious pathophysiologie consequence of drowning is

hypoxemia due to ARDS.[2] Even with early successful by-

stander CPR, ARDS with MOF is among the most eommon

delayed causes of drowning fatalities. [7]

To improve survival, ECMO has been attempted in drown-

ing victims with ARDS and hypothermia.[3] However, there is

limited data for this approach, and fatal vaseular eomplieations

related to ECMO would not be uncommon, especially with

MOF and/or bleeding diatheses. Although few eases about sue-

eessful reeovery of drowning patients with inhaled nitrie oxide

gas[8] or prone ventilatory positioning[9] has been reported,

those cases were not as detrimental as our patient. Alternative-

ly, we describe the rapid, successful treatment of ARDS with

MOF in a near drowning patient. As part of the complex

Joo Myung Lee, et al : Drowning Rescue by Prone Ventilatory Positioning 199

management, mechanical ventilation in a prone position was

critical to the patient's recovery. Coupled with use of inhaled

nitric oxide gas, this strategy seems far simpler and less risky

than ECMO and may constitute a preferred option, with

ECMO as a plan of last resort.

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