Case Reports in Critical Care最新文献

Background: Cardiogenic shock complicating peripartum cardiomyopathy (PPCM) is a rare but lethal syndrome. The etiology of PPCM is not fully elucidated and is probably multifactorial, and viral infection might play some role. It has been documented that the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) directly invades the cardiomyocytes and most commonly damages this vital organ via complex systemic devastating mechanisms. Case presentation. A 28-year-old pregnant female was admitted to a COVID-19 field hospital due to a SARS-CoV-2 infection. She gave birth by spontaneous vaginal delivery at 34 gestational weeks. Six hours after the delivery, she presented signs of hemodynamic collapse and became comatosed, requiring a transfer to the COVID-19 intensive care center. The brain magnetic resonance imaging excluded thromboembolism, intracerebral hemorrhage, and central nervous system infection and revealed a hypoxic-ischemic encephalopathy. Bedside echocardiography documented a dilated left ventricle and severely reduced left ventricular systolic function with an ejection fraction of 24%. The management was aimed at a cardiogenic shock secondary to peripartum cardiomyopathy. The clinical course was favorable: the hemodynamics stabilized, the cognitive function fully recovered, and the patient was extubated on the second day of admission to the intensive care unit. The patient was discharged from the hospital ten days after admission. Neurological and cardiovascular checkups six months after discharge showed full recovery.

Conclusion: Peripartum cardiomyopathy-induced cardiogenic shock with severe neurological consequences in COVID-19 patients was rare but did exist. A systemic approach and vigorous efforts to pinpoint the accurate diagnosis played important roles in the prompt and appropriate management.

In this case report, we describe a previously healthy eleven-year-old male diagnosed with multisystem inflammatory syndrome in children (MIS-C) associated with coronavirus disease 2019. The patient presented with shock and neurologic symptoms including altered mental status and dysarthria. Brain magnetic resonance imaging, obtained to rule out thromboembolic injury, demonstrated cytotoxic edema of the corpus callosum, an imaging finding similar in nature to several previous reports of MRI abnormalities in children with MIS-C. Following administration of intravenous immunoglobulin and pulse-dose steroids, the patient convalesced and was discharged home. Medications prescribed upon discharge included a steroid taper, daily aspirin, and proton pump inhibitor. Four days later, he was readmitted with shock and life-threatening gastrointestinal (GI) hemorrhage. After extensive evaluation of potential bleeding sources, angiography revealed active bleeding from two arterial vessels supplying the duodenum. The patient demonstrated no further signs of bleeding following successful coil embolization of the two vessels. We hypothesize that the vasculitic nature of MIS-C combined with anti-inflammatory and antithrombotic therapy placed him at risk of GI hemorrhage. This case highlights unique radiologic features of MIS-C as well as potential complications of treatment.

Introduction: Aluminum phosphide (rice tablet) was first introduced as a pesticide in India. Rice tablets are commonly used in Iran due to their high efficacy against rodents and insects, low cost, and availability. Aluminum phosphide is a lethal poison without antidote and causes cardiocirculatory collapse and has negative inotropic cardiac effect. Human and animal studies showed that high dose insulin had positive cardiac inotropic effects. GIK (glucose, insulin, and potassium) assists heart uptake of carbohydrates that are the major fuel substrate of the myocard muscle under stressed conditions and leading to correction of acidosis, increased myocardial contractility, and peripheral vascular resistance. Case Presentation. In this manuscript, a young woman with aluminum phosphide poisoning was described to have presented with hypotension, hypoxemia, and severe metabolic acidosis. In contrast to our previous experiences that approximately all rice tablet poisoning patients with shock were dead despite full conservative treatment, this patient miraculously was saved with high dose intravenous regular insulin infusion and was discharged from the hospital with good condition and without any complications.

Conclusion: Rice tablet poisoning has high fatality rate, and to date, no antidote is available. GIK is suggested as a potential life saving treatment for critical rice tablet poisoning patients with symptoms and signs of shock.

Point-of-care ultrasound (POCUS) is becoming a frequently utilized imaging tool in the emergency department (ED) as it can aid in early diagnosis of many pathologies. This is a case report of a 55-year-old male who presented to the emergency department by ambulance for sudden onset chest pain followed by a syncopal episode. Point-of-care echocardiogram revealed a large pericardial effusion with a significantly dilated aortic root, concerning for aortic dissection. Patient was emergently taken for a computed tomography (CT) scan, which was only remarkable for an ascending thoracic aortic aneurysm but failed to show an aortic dissection flap. On repeat POCUS, a dissection intimal flap, large pericardial effusion with tamponade physiology, and aortic regurgitation were identified and later confirmed on transesophageal echocardiogram. This case report details a rare pathology that was correctly identified on initial POCUS before it was seen on CT scan.

Symmetrical peripheral gangrene (SPG) is a rare clinical syndrome characterized by an acute onset of ischemic damage in two or more extremities without obstruction or vasculitis of supplying vessels. Body parts commonly affected include toes, hands, scrotum, and earlobes, increasing the risk of limb amputation and impairing the quality of life. The vascular injury mechanism is disseminated intravascular coagulation. SPG may manifest unpredictably in conditions associated with septic shock, low output states, vasospastic conditions, myeloproliferative disorders, or hyperviscosity syndrome. A review on the topic is presented based on a 3-case series of SPG that required amputation of fingers and toes after the administration of vasopressors in a septic shock context.

Remdesivir (RDV) is an approved treatment for hospitalized patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. There is limited literature on the cardiac adverse effects of RDV. We report a case of a patient who developed hemodynamically unstable bradycardia after the initiation of RDV that resolved after discontinuing RDV.

Background: Lactic acidosis is a well-known complication of metformin accumulation in diabetic patients with kidney failure. However, it is not usual to raise the diagnosis of metformin-associated lactic acidosis when patients have normal kidney function. The causes of metformin-induced high lactate include the accumulation of normal doses of metformin in chronic kidney disease, an overdose of this drug without kidney failure, or an increase in lactate production due to the inhibition of liver gluconeogenesis. Case Presentation. We report the case of a 61-year-old diabetic man who was brought to the emergency room in a comatose state. His family reported abdominal pain with diarrhea in the last two days. He was found to have severe lactic acidosis with normal serum creatinine. He was on a regular dose of metformin, and his family denied any other medical history or any alcohol abuse. He showed no signs of infection, his liver enzymes were slightly elevated, and he had severe anemia. His hemodynamics deteriorated quickly within hours, and an abdominal computed tomography scan revealed no abnormalities. He underwent a laparotomy that ruled out mesenteric ischemia and revealed an abnormal liver. The liver biopsy later confirmed the diagnosis of cirrhosis.

Conclusions: We discuss here the probable causes of severe lactic acidosis and the role of metformin in exacerbating this acid-base disturbance in cirrhotic patients. Future research is needed to determine whether these patients might benefit from dialysis.

Plasmapheresis for the treatment of hypertriglyceridemia is relatively uncommon and mostly reported either in patients experiencing hypertriglyceridemia-induced acute pancreatitis or patients with therapy-resistant familial hypercholesterolemia. Standard therapies for hypertriglyceridemia include dietary modification and lipid-lowering medication. For severe hypertriglyceridemia, the risk of pancreatitis increases significantly as triglyceride levels increase above 1000 mg/dL, and current therapies are unable to reduce triglyceride levels rapidly enough. Here, we report a case of a 48-year-old male patient who presented to the emergency department due to an amitriptyline overdose. In addition to being started on IV sodium bicarbonate therapy, an intravenous 20% fat emulsion bolus at 1.5 mL/kg was administered followed by 0.25 mL/kg/min infusion for 4 hours as a strategy to absorb lipophilic amitriptyline. Two days posttreatment, he was noted to have substantial hypertriglyceridemia (serum triglycerides: 6,475 mg/dL). His amylase was within the normal range at 37 U/L (reference range: 20-100 U/L), his lipase was low at 40 U/L (reference range: 75-390 U/L), and he was without evidence of any clinical sequelae secondary to hypertriglyceridemia (e.g., pancreatitis). Due to the severity of his hypertriglyceridemia, plasmapheresis was initiated urgently for rapid reduction in serum triglyceride levels to prevent pancreatitis and end-organ damage. He underwent a 1-plasma volume exchange with 5% albumin as the replacement fluid. This reduced his triglyceride levels to 185 mg/dL (reference range: 3-149 mg/dL). His symptoms secondary to his amitriptyline overdose were also resolved. Here, we report a 2-step process of intravenous lipid emulsion followed by plasmapheresis for amitriptyline overdose.

Background: Restless leg syndrome (RLS) is a common neurological condition that manifests as creeping, nonpainful urges to move lower extremities and is relieved with movements of the legs. RLS is associated with comorbidities such as gastric surgery, diabetes mellitus, uremia, and iron deficiency anemia, and it is misdiagnosed in many cases. Drugs like levodopa, ropinirole, pramipexole, cabergoline, and pergolide that target the dopaminergic system have been traditionally used to treat symptoms of RLS. α2-adrenoceptor (α2-AR) agonists, like clonidine and dexmedetomidine, have also been reported to show improvement of RLS symptoms during sedation. Specific Aim. This case report suggests that dexmedetomidine may have worsened RLS during sedation in a 71-year-old male with no prior diagnosis of RLS or reported symptoms. The patient had a procedure for right first metatarsophalangeal joint (MTPJ) fusion, with second digit proximal interphalangeal joint (PIPJ) arthrodesis, and flexor tendon transfer due to pain on walking and failing conservative therapy. He underwent intravenous sedation/monitored anesthesia care (MAC) with propofol, dexmedetomidine, and a peripheral regional block for intraoperative anesthesia and postoperative analgesia. During the surgery, the patient experienced continuous bilateral leg movement, unpredictable, and unrelated to surgical stimulation or level of consciousness within 5 minutes of administration of dexmedetomidine. The patient tolerated the procedure, and the unpredicted leg movement was managed by the surgeons intraoperatively.

Conclusion: Although no previous literature exists and mechanisms are unclear, this case report hypothesizes that dexmedetomidine may contribute to worsening RLS symptoms.

Methylenedioxymethamphetamine (MDMA) is a psychoactive substance that is used commonly as a recreational drug at rave music festivals. MDMA intoxication can cause a myriad of symptoms and side effects including the manifestation of hyperpyrexia in patients. Hyperpyrexia can mimic a heat stroke and ultimately lead to various forms of end-organ damage. The most common methods used in treating MDMA-induced hyperpyrexia focus on the rapid reduction of core body temperature. Various off-label medications have also been used in combating MDMA-induced hyperpyrexia. Dantrolene is one such medication, although its role in the treatment of MDMA intoxication remains uncertain. This case series preliminarily examines the efficacy of dantrolene in mitigating MDMA-induced hyperpyrexia and potentially reducing the risk of end-organ damage in patients suffering from MDMA overdose. This study focuses on nine patients who presented after ingesting various forms of MDMA at "rave" music events. All patients were found to be hyperthermic in the field with a maximum core body temperature of 109 degrees Fahrenheit. All patients were immediately managed by cooling measures, and seven patients additionally received dantrolene in the field before being transferred to Arrowhead Regional Medical Center. Upon arrival to the hospital, nearly every patient was found to have significantly decreased body temperatures when compared to previously measured body temperatures out in the field. However, nearly all patients in the study were also noted to have laboratory abnormalities consistent with various forms of end-organ damage. The degree and severity of end-organ damage observed in MDMA-induced hyperpyrexia seem to be a function of initial core body temperature. Higher core body temperature tends to correlate with more forms of end-organ damage and a higher severity of end-organ damage. Intervention with dantrolene and cooling measures appeared to have no effect on reducing the risk of developing end-organ damage in this patient population.