CARDIOGENIC SHOCK AND GLOBUS PALLIDUS INJURY AS A PRESENTATION OF CARBON MONOXIDE POISONING

SUMMARY

Carbon monoxide poisoning is one of the leading causes of mortality and morbidity by poisoning in the world. Signs and symptoms are nonspecific and related to impaired oxygen delivery to tissues, with the brain being the most affected organ due to its high oxygen demand. CO-Hb is a poor indicator of severity and long-term outcome, with clinicians relying more on clinical features such as level of consciousness and need for intubation, organ dysfunction and shock and also pH level. A 45-year-old female was found unconscious in her home with the fireplace lit and smoke all over the house. She was last seen well 18 hours before. She was brought to the emergency department and was admitted to the ICU in coma and cardiogenic shock, with a metabolic acidosis with hyperlactacidemia and a CO-Hb level of 15.5%. Laboratorial investigation revealed hepatic cytolysis, acute renal failure, rhabdomyolysis and a troponin I level of 338 ng/L. ECG showed no acute myocardial ischemia. Echocardiogram revealed diffuse hypokinesia with an ejection fraction of 25%. Head CT scan showed bilateral and symmetrical hypodensities of the globus pallidus. The patient underwent hyperbaric oxygen treatment with full neurological and cardiac recovery, allowing extubation 48 hours after admission. This rare severe case of coma due to carbon monoxide intoxication with globus pallidus injury and cardiogenic shock was successfully treated with hyperbaric oxygen, showing that it can be the right treatment choice in these cases, with an excellent impact on neurological and cardiac outcome.

Introduction

Carbon monoxide (CO) poisoning, or the “silent killer”, is responsible for up to 2000 accidental deaths each year in the US.¹ The toxicity of CO is linked to almost 250 times greater affinity of CO for haemoglobin than of oxygen, leading to insufficient oxygenation at the tissue level. CO has also a high affinity to myoglobin in myocardium and inhibits the activity of cytochrome c oxidase, resulting in cardiac and neurologic dysfunction.² The typical clinical presentation includes headache, dizziness, nausea and vomiting, fatigue, seizures and coma. Cardiac involvement is less frequent and mainly related to arrhythmia, angina, myocardial infarction and left ventricular dysfunction, with cardiogenic shock and sudden death being rare.³ There is no reliable marker of severity of poisoning. CO-Hb levels are not a good indicator of severity or long-term outcome. Since neurologic and cognitive sequelae are common in CO poisoning, hyperbaric oxygen treatment should be offered to severely poisoned patients in intensive care as it is linked to a reduction in cognitive sequelae.^4,5 We present a case of carbon monoxide poisoning that was admitted to intensive care due to coma with globus pallidus injury and cardiogenic shock, treated with hyperbaric oxygen with full recovery of cardiac and neurologic functions.

Case presentation

A 45-year-old female with no previous past medical history was admitted to the emergency department in coma, found in her home, last seen well 18 hours before. At her home the pre-hospital team found the fireplace lit and smoke all over the house. Physical examination revealed Glasgow coma scale (GCS) of 7 (e1, v2, m4), blood pressure of 93/59 mmHg, heart rate of 130 bpm, with no respiratory distress. Arterial blood gas with non-rebreather mask showed pH 7.35, pCO2 27.1 mmHg, pO2 482 mmHg, HCO3 15 mmol/L, SaO2 99%, CO-Hb 15.5%, lactate 5.47 mmol/L.

Chest X-ray revealed diffuse interstitial involvement. ECG with sinus tachycardia. Laboratorial investigation showed haemoglobin 12.8 g/dL, leukocytes 17500/μL, platelets 328000/μL, AST 199 >20U/L, ALT 62 >20U/L, LDH 500 >302U/L, urea 63.8 >20mg/dL, creatinine 1.45 >0.56mg/dL, troponin I 338 >74ng/L, CK 13512 >379 U/L, CK-MB 525 >267U/L, myoglobin 7814 >718ng/mL. Toxicology screen was negative.

Head CT scan showed bilateral and symmetrical hypodensities of the globus pallidus (Fig. 1).

Fig. 1.

Head CT scan showing bilateral and symmetrical hypodensities of the globus pallidus

The patient was admitted to the ICU with the diagnosis of coma due to carbon monoxide poisoning, rhabdomyolysis, in circulatory shock and acute renal failure. She was intubated and mechanically ventilated, under noradrenaline (NAD) support (0.46 mcg/kg/min).

Echocardiogram revealed diffuse hypokinesia with an ejection fraction of 25%, LVOT VTi 7 cm, inferior vena cava 20 mm without significant variability, no right-sided heart chambers dilatation or pericardial effusion.

Transpulmonary thermodilution monitoring was inserted, confirming the diagnosis of cardiogenic shock: CI 2.5 0 l/min/m², GEF 19%, SVRI 2800 dyn.s.cm.⁵.m², GEDI 500 mL/m², EVLWI 7 mL/Kg. A bolus of 500 mL of crystalloids was initiated and dobutamine was started with a consistent improvement in cardiac function, urinary output and recovery of acute renal failure with a decrease in the dose requirement of NAD and lactate washout.

Two sessions of hyperbaric oxygen treatment were completed with CO-Hb level decreasing from 15 to 0.1% and the patient had a full recovery with no organ dysfunction. Complete neurological recovery allowed a successful extubation and the follow up echocardiogram showed an ejection fraction superior to 50% without vasoactive support.

Discussion

Tissue hypoxia is the main toxic effect of acute CO poisoning, which is explained by the formation of CO-Hb stable complex and direct carbon monoxide-mediated damage at the cellular level. The brain is a high oxygen demand organ, thus especially sensitive to impaired oxygen delivery. Cardiac output should increase in order to maintain oxygen delivery to the brain. In the beginning, the hypoxia leads to a compensatory tachycardia which increases the oxygen demand and accelerates CO diffusion, further increasing the hypoxic injury to the myocardium. Besides that, CO poisoning has also a direct effect in myocardium, binding to myoglobin and inhibiting the activity of cytochrome oxidase, reducing the oxygen supply to the mitochondria, leading to anaerobic metabolism with production of free radicals and lactate.^4,6-8 This effect and a concomitant reperfusion injury caused by CO washout and restauration of aerobic metabolism may justify the myocardial stunning which induces a negative inotropic effect on myocytes, leading to cardiogenic shock seen in our patient. Younger patients as in our case with no cardiovascular risk factors are more linked to diffuse left ventricular dysfunction, whereas older patients may be more prone to present with segmental hypokinesis. Either way, myocardial dysfunction is a significant predictor of mortality.⁹

Head CT scan showed bilateral and symmetrical injury of the globus pallidus, the most common site of immediate involvement in CO poisoning.^10-12 This can be explained by the fact that globus pallidus and substantia nigra are the brain regions with the highest iron content, leading to a direct binding of the carbon monoxide to heme iron. It can also indicate that globus pallidus necrosis may be preferentially vulnerable to hypoxic-ischemic injury because it is supplied by perforating lenticulostriate branches of the middle cerebral artery, branches from anterior cerebral artery and also from the anterior choroidal artery.

There is still some debate concerning the use of hyperbaric oxygen therapy.¹³ Since CO-Hb levels do not have a good correlation with severity and long-term outcome, clinicians must rely more on clinical features such as level of consciousness, need for intubation, pH level, organ dysfunction and cardiovascular damage as a criteria for hyperbaric oxygen therapy.^5,14 Our patient had many poor prognostic factors: metabolic acidosis, persistent low GCS with the need to intubate, multiple organ dysfunction and cardiogenic shock. However, the outcome was excellent due to prompt and correct diagnosis, proper organ support and hyperbaric oxygen treatment.

Conclusions

We present a case that illustrates an atypical initial presentation of carbon monoxide poisoning consisting of coma with globus pallidus injury and cardiogenic shock, treated successfully with hyperbaric oxygen with no neurological and cardiac sequelae. We suggest that in cases of severe carbon monoxide poisoning, regardless the initial levels of CO-Hb, patients should undergo a rational screening for cardiac disfunction and be considered for early hyperbaric oxygen therapy, with an impact on patient outcome.