==== Front Cureus Cureus 2168-8184 Cureus 2168-8184 Cureus Palo Alto (CA) 10.7759/cureus.39729 Emergency Medicine Internal Medicine Substance Use and Addiction Unusual Presentation and Outcome in Acute Cocaine Intoxication With Multiorgan Failure: A Case Report Muacevic Alexander Adler John R Kim Andrew G 1 Watat Kevin 1 Ghnaima Harith 1 Yavari Majid 1 Rayamajhi Supratik 1 1 Internal Medicine, Michigan State University, East Lansing, USA Andrew G. Kim andykimheart@gmail.com 30 5 2023 5 2023 15 5 e3972930 5 2023 Copyright © 2023, Kim et al. 2023 Kim et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. This article is available from https://www.cureus.com/articles/156346-unusual-presentation-and-outcome-in-acute-cocaine-intoxication-with-multiorgan-failure-a-case-report Cocaine overdose remains a significant public health concern worldwide, with potentially life-threatening consequences. The range of presentation can vary from mild autonomic hyperactivity to severe vasoconstriction, causing multiorgan ischemia and even death. In cases of high-dose intoxication, the presentation can be atypical. In this case report, we present a compelling case of a patient who initially presented with cardiac arrest and atypical signs. The patient made a remarkable recovery and returned almost to her baseline. This case provides valuable prognostic insight into the outcomes of severe multiorgan failure resulting from cocaine toxicity. drug induced hepatitis ischemic cardiomyopathy acute decompensated systolic heart failure vasospasm acute ischemic cerebral infarction ischemic cerebrovascular disease ischemic stroke diffuse cerebral edema multiorgan system failure acute cocaine intoxication ==== Body pmcIntroduction Cocaine overdose is a prevalent cause of acute intoxication-related emergency department visits worldwide [1]. This condition results in vasoconstriction, which leads to ischemic injury in multiple organs. However, the injury can be reversible following vasodilation [2, 3]. Here, we present a case of severe multiorgan failure resulting from acute cocaine intoxication. The patient needed intensive care unit admission for intubation, mechanical ventilation, and vasopressor support. After discharge and outpatient follow-up, the patient's organ function and residual disabilities almost fully recovered to their baseline. This case highlights that ischemic injuries caused by cocaine intoxication can spontaneously resolve, despite presenting as critical initially. Case presentation A 29-year-old female patient with a history of anxiety disorder and polysubstance use disorder, including alcohol consumption, marijuana smoking, and occasional cocaine snorting over the past couple of years, was brought to the emergency department after experiencing a cardiac arrest. She had snorted an excessive amount of cocaine and had reported headaches and chest pain before losing consciousness. Upon the arrival of emergency medical services, she was in a pulseless electrical activity, but spontaneous circulation was returned after four rounds of cardiopulmonary resuscitation. In the emergency department, she remained unresponsive, with vital signs of blood pressure 78/43 mmHg, heart rate of 96 beats per minute, and core body temperature of 90.7°F (32.6°C) on a warm summer day in August in Michigan. Her pupils were fixed at 3 mm and showed no reaction to light. The patient was intubated, mechanically ventilated, given intravenous fluid boluses, and transferred to the intensive care unit. The laboratory results showed an arterial pH of 7.19, lactate of 2.7 mmol/L, creatinine of 2.72 mg/dL, troponin I of 5190 ng/mL, creatine phosphokinase (CPK) of 5855 mcg/L, lactate dehydrogenase (LDH) of 4,219 IU/L, aspartate aminotransferase (AST) greater than 10,000 U/L, alanine transaminase (ALT) of 4600 U/L, and a positive urine drug screen for cocaine and benzoylecgonine consistent with cocaine intoxication. Cortisol levels were not evaluated, and microbiological cultures yielded negative results (Table 1, Figure 1). Table 1 The initial laboratory values upon admission Significant results include troponin I high sensitivity of 5190 pg/mL, AST of >10,000 U/L, ALT of 4600 U/L, and creatinine of 2.72 mg/dL. WBC - white blood cell count, RBC - red blood cell count, MCV - mean corpuscular volume, MCH - mean corpuscular hemoglobin, MCHC - mean corpuscular hemoglobin concentration, RDW - red cell distribution width, MPV - mean platelet volume, BUN - blood urea nitrogen, PCO2 - partial pressure of carbon dioxide, PO2 - partial pressure of oxygen, O2 - oxygen, FiO2 - fraction of inspired oxygen, CPK - creatine phosphokinase, LDH - lactate dehydrogenase, AST - aspartate aminotransferase, ALT - alanine aminotransferase Analysis Result Reference range Complete blood count WBC 22.6 4.0 - 12.0 10^3/µL RBC 3.89 3.50 - 5.55 10^6/µL Hemoglobin 11.4 12.0 - 15.0 g/dL Hematocrit 34.2 36.0 - 45.0 % MCV 88 80 - 100 fL MCH 29.3 27.0 - 33.0 pg MCHC 33.3 31.0 - 37.0 g/dL Platelet 41 150 - 400 10^3/µL RDW 15.2 11.6 - 14.6 % MPV 7.8 7.3 - 11.5 fL Differential Neutrophils 93.6 49.0 - 81.0 % Lymphocytes 4.8 14.0 - 41.0 % Monocytes 1.5 0.0 - 11.0 % Eosinophils 0 0.0 - 6.0 % Basophils 0.1 0.0 - 3.0 % Absolute neutrophils 21.1 1.96 - 9.72 10^3/µL Absolute lymphocytes 1.1 0.56 - 4.92 10^3/µL Absolute monocytes 0.3 0.00 - 1.32 10^3/µL Absolute eosinophils 0 0.00 - 0.72 10^3/µL Absolute basophils 0 0.00 - 0.36 10^3/µL Chemical profile Sodium 141 135 - 145 meq/L Potassium 4.8 3.5 - 4.9 meq/L Chloride 112 96 - 110 meq/L Bicarbonate 16 20.0 - 32.0 mmol/L Anion gap  13 16-Feb Glucose 85 65 - 99 mg/dL BUN 35 6 - 23 mg/dL Creatinine 2.72 0.60 - 1.40 mg/dL Magnesium 2.2 1.6 - 2.5 mg/dL Calcium 7.44 8.00 - 10.50 mg/dL Ionized calcium 1.11 1.10 - 1.30 mmol/L Phosphorus 6.7 2.5 - 4.5 mg/dL Albumin 3 3.6 - 5.0 g/dL Total protein 5.1 6.0 - 8.0 g/dL Arterial blood gas pH 7.19 7.35 - 7.45 PCO2 35 34 - 46 mmHg PO2 96 75 - 100 mmHg Bicarbonate 12.6 20 - 30 mmol/L Base excess -14.6   O2 saturation 96.5 95 - 98 % FiO2 30%   Cardiac profile CPK 5,855 0 - 155 U/L LDH 4,219 100 - 225 U/L Troponin I high sensitivity 5,190 0 - 18 pg/mL B-natriuretic peptide 111 0 - 100 pg/mL Liver profile AST >10,000 10 - 40 U/L ALT 4,600 3 - 45 U/L Total bilirubin 0.5 0.2 - 1.2 mg/dL Direct bilirubin 0.3 0.0 - 0.3 mg/dL Alkaline phosphatase 82 37 - 98 U/L Ammonia 123 13 - 37 µmol/L Lactate 2.7 0.2 - 1.8 mmol/L Urinalysis Type Unspecified   Color Yellow Yellow Clarity Slightly cloudy Clear Glucose Negative Negative Ketones Negative Negative Blood Large Negative Nitrites Positive Negative Leukocyte esterase Negative Negative pH 6 4.5 - 8.5 Bilirubin Negative Negative Urobilinogen Negative Negative Urine microscopy WBC 10-Jun 0 - 5 RBC 20-Nov 0 - 3 Bacteria Few None Squamous cells Occasional   Urine toxicology Barbiturates Negative 200 ng/mL Cannabinoids Negative 20 ng/mL Cocaine Positive 300 ng/mL Opiates Negative 300 ng/mL Phencyclidine Negative 25 ng/mL Methadone Negative 300 ng/mL Benzodiazepines Negative 200 ng/mL Benzoylecgonine Positive 30 ng/mL Amphetamines/methamphetamines Negative 1000 ng/mL Tricyclinc antidepressants Negative 300 ng/mL Oxycodone Negative 50 ng/mL Ecstasy Negative 500 ng/mL Specimen validation pH 6.5   Specimen validation specific gravity 1.025   Figure 1 A chest X-ray taken shortly after the patient's arrival at the hospital, following endotracheal intubation and the insertion of a central line The chest X-ray showed no signs of acute abnormalities. Despite the patient experiencing an initial out-of-hospital cardiac arrest, targeted temperature management to induce therapeutic hypothermia was not initiated due to the patient already having been hypothermic for the initial 24 hours. Additionally, therapeutic alpha-blockers to address cocaine-induced vasoconstriction were not administered due to severe hypotension. Initially, the patient was completely unresponsive without any sedation, but later sedation was started when the patient began exhibiting autonomic hyperactivity. The initial CT and CT angiogram of the brain showed diffuse cerebral edema and multiple infarctions in the bilateral middle and posterior cerebral arteries, most prominent in the left middle cerebral artery territory on the CT scan (Figure 2). The initial echocardiogram showed a left ventricular ejection fraction of less than 20%, with diffuse severe hypokinesis and akinesis. The patient's renal function continued to decline for the first three days, and continuous renal replacement therapy was initiated. Later, when the patient's hemodynamic status improved, a tunneled dialysis catheter was inserted to begin hemodialysis. Figure 2 The CT and CT angiogram of the head upon admission Left: The CT scan of the head revealed infarction in the middle cerebral artery territory, with the left hemisphere (Arrows) affected more than the right. Right: The CT angiogram revealed opacification of the bilateral proximal middle cerebral arteries (upward arrows) and posterior cerebral arteries (downward arrows). However, on the follow-up echocardiogram on day three, the ejection fraction significantly improved to 70-75%, and the wall motion abnormalities resolved spontaneously. On day four, an MRI showed that the diffuse cerebral edema and multiple infarctions in the cerebral arteries visible on the initial CT scan had spontaneously resolved (Figure 3). After being extubated, the patient exhibited significant weakness in her right arm, likely as a result of a temporary infarction in the left middle cerebral artery. However, this focal weakness fully resolved over time with physical therapy. Despite initial severe shock liver, the patient's liver function tests had also rapidly improved without signs of decompensation. Figure 3 Follow-up MRI of the brain on day four The initial findings of diffuse cerebral edema and infarctions, as depicted in Figure 2, have resolved. Left: T2-weighted image; Middle: diffusion-weighted image; Right: apparent diffusion coefficient image The patient's acute kidney injury persisted in the context of shock kidneys and rhabdomyolysis. On day 17, the patient was discharged with a plan to receive scheduled outpatient hemodialysis for the ongoing treatment of her acute kidney injury. However, during the follow-up, the patient's acute kidney injury had completely resolved as well, and the dialysis catheter was removed. Discussion Cocaine inhibits the neuronal uptake of norepinephrine, which in turn stimulates adrenergic receptors, leading to vasospasm and sympathomimetic overstimulation [2, 3]. It also blocks sodium channels and possesses local anesthetic properties [4]. Cocaine can lead to ischemic organ failure either through cardiogenic shock [5] or by inducing direct vasospasm of the vasculature supplying the target organ [6, 7]. Stimulation of alpha-adrenergic receptors of coronary artery smooth muscle cells induces coronary artery vasospasm and vasospastic angina [8], which the patient likely experienced before cardiac arrest. Nevertheless, cocaine can occasionally result in acute ischemia in different organs by causing thromboembolism as well [9]. Typical signs of cocaine overdose include hypertension, tachycardia, and hyperthermia. However, clinicians need to be cautious because, in cases of high-dose intoxication, patients may present with the opposite signs of hypotension and bradycardia due to severe ischemic multiorgan failure [10]. Hypothermia is a rare occurrence in patients with cocaine overdose, particularly during the summer. Although animal studies have demonstrated that cocaine can induce hypothermia [11], it has rarely been reported in human subjects. Fuller et al. (2008) also presented a patient who experienced initial hypothermia and cardiac arrest due to massive cocaine intoxication, but therapeutic hypothermia was induced to further lower the patient's body temperature. Similar to our case, this patient had nearly complete neurological recovery [12]. In order to determine the extent of this phenomenon, it is considered essential to have more case reports or case series that involve human subjects. Therapeutic hypothermia is often utilized in patients who experience cardiac arrest, and the initial hypothermia observed in our case likely contributed to the positive outcome [13].  Conclusions Acute cocaine intoxication commonly presents with signs of hypertension, tachycardia, and hyperthermia. However, high-dose intoxication may result in atypical symptoms like hypotension, bradycardia, and hypothermia, as demonstrated in this case. Hypothermia in humans with cocaine overdose is rarely reported and requires further investigation. Cocaine can cause severe ischemic multiorgan failure and even death. Nevertheless, vasospasm triggered by cocaine use is reversible, which might explain why the prognosis for the patient with severe ischemic multiorgan failure due to cocaine overdose was surprisingly favorable when compared to other causes. Human Ethics Consent was obtained or waived by all participants in this study The authors have declared that no competing interests exist. ==== Refs References 1 The global burden of disease attributable to alcohol and drug use in 195 countries and territories, 1990-2016: a systematic analysis for the Global Burden of Disease Study 2016 Lancet Psychiatry GBD 2016 Alcohol and Drug Use Collaborators 987 1012 5 2018 30392731 2 Cocaine use and the likelihood of nonfatal myocardial infarction and stroke: data from the Third National Health and Nutrition Examination Survey Circulation Qureshi AI Suri MF Guterman LR Hopkins LN 502 506 103 2001 11157713 3 Cardiovascular complications of cocaine use N Engl J Med Lange RA Hillis LD 351 358 345 2001 11484693 4 Cocaine: What is the crack? A brief history of the use of cocaine as an anesthetic Anesth Pain Med Redman M 95 97 1 2011 25729664 5 Transient left ventricular acute failure after cocaine use Curr Drug Res Rev Cardinale M Esnault P Schmitt J Meaudre E 142 144 11 2019 31333135 6 Cocaine and vasospasm N Engl J Med Isner JM Chokshi SK 1604 1606 321 1989 2586556 7 Cocaine-induced vasospasm causing spinal cord transient ischemia Neuroradiol J Gorelik N Tampieri D 364 367 25 2012 24028991 8 Cocaine and cardiotoxicity: A literature review Cureus Pergolizzi JV Jr Magnusson P LeQuang JA Breve F Varrassi G 0 13 2021 9 Cocaine: A provoking risk factor in venous thromboembolism Cureus Griffin D Cha S 0 11 2019 10 Cocaine-induced bradyarrhythmias Am Heart J Om A Ellenbogen KA Vetrovec GW 232 234 124 1992 1615817 11 Cocaine alters body temperature and behavioral thermoregulatory responses Neuroreport Gonzalez LP 106 108 4 1993 8453030 12 Therapeutic hypothermia in cocaine-induced cardiac arrest Ann Emerg Med Fuller ET Milling TJ Jr Price B Spangle K 135 137 51 2008 18036703 13 Accidental hypothermia: 2021 update Int J Environ Res Public Health Paal P Pasquier M Darocha T 501 19 2022 35010760