K Katyayani and R Kapoor present a case study of severe hypothermia, complicated by cardiac arrest secondary to accumulation of uremic toxins in a patient with known stage four kidney disease secondary to renovascular hypertension
Summary
Uremic syndrome is known to occur in patients with advanced kidney disease and one of the presenting symptoms, apart from fluid and electrolyte imbalance, can be hypothermia. What is uncommon though is the primary presentation of uremic syndrome being profound hypothermia. We report a case of severe hypothermia complicated by cardiac arrest secondary to accumulation of uremic toxins in a patient with known stage 4 kidney disease secondary to renovascular hypertension. This case emphasises the need to be vigilant, especially in elderly patients with chronic renal disease, who are at higher risk of suffering from age-related impairments to their thermoregulatory system and therefore more likely to present with hypothermia complicating uremia. Uremic syndrome, despite being a rare cause of hypothermia, with early diagnosis and effective management can lead to excellent patient recovery within a short space of time.
Introduction
Uremic syndrome is a manifestation of end stage kidney disease and, as such, most patients are commenced on renal replacement therapy long before the clinical signs and symptoms of uremic syndrome manifest. This makes patients presenting acutely with uremic syndrome a somewhat uncommon occurrence. Although hypothermia is associated with uremic syndrome, severe hypothermia is rare. Humans have a remarkable ability to maintain a relatively constant core body temperature of 36.5-37.5°C, irrespective of the environment due to the presence of an effective thermo-regulatory system. Severe hypothermia i.e. a temperature below 28° C can cause significant morbidity and mortality. The causes are varied with exposure to cold stress, especially during winter being one of the commonest. Other causes include sepsis, endocrine disorders, hypoglycaemia and DKA. Though the pathophysiology and management of uremic syndrome has been extensively researched, the evidence regarding hypothermia in uremic syndrome is limited. Accumulation of Endogenous cryogens in uremic syndrome has been thought to induce peripheral vasodilatation and supress shivering metabolism, thus inducing falls in body temperatures [1]. We report a case of a patient with known stage 4 kidney disease secondary to reno-vascular hypertension who presented with hypothermia and suffered a cardiac arrest which were both secondary to accumulation of uremic toxins.
Description
A 60-year-old retired gentleman was brought into accident and emergency by ambulance with worsening confusion and reduced responsiveness. He had a body mass index (BMI) of 42, a background history of hypertension, and chronic kidney disease (CKD) stage 4 secondary to hypertension induced renovascular disease. He was noncompliant with his regular antihypertensive medications, which included calcium channel blockers and beta blockers. He was also non-compliant with nephrology appointments.
On presentation, he was bradycardic with a heart rate between 30-35 beats/min and hypotensive. Although his GCS was 11/15 (E3V3M5) he was profoundly hypothermic with a temperature of 280 C with a tympanic thermometer. The hypothermia was not associated with shivering. There was no history of exposure to cold environment to explain the finding of severe hypothermia.
Arterial blood gas done on arrival confirmed a significant metabolic acidosis with a lactate of 7.7 mmol/L.
Active rewarming was commenced with forced air warming device. In view of the hypotension, 500 micrograms of intravenous atropine was administered, but no response to the heart rate was noted. In addition to supplemental oxygen and warm fluid resuscitation, routine blood tests including a full blood count, electrolytes and renal and liver function tests were requested. Over the next thirty minutes he became unresponsive and suffered a witnessed asytolic cardiac arrest. Cardio pulmonary resuscitation (CPR) was commenced immediately and return of spontaneous circulation was achieved after two cycles of CPR and 1 mg intravenous adrenaline. He immediately regained consciousness and could maintain a patent airway throughout, though he remained bradycardic and hypotensive with worsening metabolic acidosis. The patient also received one dose of empirical broad-spectrum antibiotics as sepsis was considered as one of the differential diagnosis. He was noticed to be anaemic with an Hb of 60 gm/L and in acute kidney injury with a urea of 48mmol/L and creatinine of 1099 mmol/L.
He was transferred to the intensive therapy unit (ITU), where invasive monitoring and inotropes were commenced with active rewarming continued. As his blood pressure stabilised on inotropes he was commenced on continuous veno-venous hemofiltration (CVVHF). A focused bedside echocardiography was performed to rule out cardiogenic shock and confirmed well-functioning right and left ventricles with no evidence of pericardial effusion.
On renal replacement therapy over the next 10 hours his heart rate spontaneously recovered to 86 beats/min. Antibiotics were discontinued as the infective markers were within normal limits and no focus of infection was identified. Over the following 12 hours his temperature normalised, inotropes were weaned off, he was tolerating oral intake, but remained on CVVHF. During his stay on the ITU septic screen, thyroid function tests, random cortisol levels and trans-thoracic echocardiography were all within normal limits. His illness and brief cardiac arrest were attributed to hypothermia and bradycardia secondary to uremic syndrome.
He made a good recovery and was discharged to the renal ward following a 44-hour stay on ITU. He was continued on regular haemodialysis and was discharged home after nine days of stay in hospital. He currently remains on regular haemodialysis and continues to do well.