CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 42 AFRICA mental confusion (Table 1). She was placed on inotropic support with an adrenaline infusion. A repeat ECG recording performed one hour after commencement of the adrenaline infusion (seven hours after initial assessment) showed ST-segment elevation in leads V3–V6 with reciprocal ST-segment depression in aVR (Fig. 2). The patient was treated as having an acute ST-elevation myocardial infarction (STEMI) and was given aspirin 300 mg and clopidogrel 300 mg orally as well as enoxaparin 30 mg intravenously, and the internal medicine team was consulted. A type II myocardial infarction was suspected in view of the temporal relationship between the initiation of adrenaline and the development of the ECG changes. In the absence of markers of sepsis (normal white cell count and C-reactive protein = 6 mg/l) the internal medicine team considered a metabolic cause for the acidosis and made a diagnosis of type B lactic acidosis secondary to thiamine deficiency, and thiamine 300 mg was administered intravenously. The decision was made to continue observing the patient while on inotropic support after thiamine had been administered. Four hours after intravenous thiamine administration, the ST-segment elevation on the ECG subsided and T-wave inversion appeared in the precordial leads V1–4 (Fig. 2). Repeat troponin I estimations remained elevated (1 275 ng/l). The patient’s inotrope requirement gradually decreased and she was fully weaned off adrenaline infusion after 24 hours. Her level of consciousness also returned to normal over 24 hours. The lactic acidosis steadily improved after intravenous thiamine and had completely resolved 27 hours after commencing thiamine (Table 1). At this stage, it was also noticed that the patient developed jaundice with worsening derangements in the liver enzymes. Repeat estimation 72 hours later showed that these also had largely resolved while receiving daily thiamine. Upon discharge, the patient disclosed that she did take alcohol, but was guarded about the type and amount of alcohol she had been consuming (probably due to the South African lockdown regulations during the COVID pandemic, which prohibited the purchase/brewing of alcohol at that time). Case report 2 A 42-year-old black male presented in extremis at 21:40 to the ED of a regional-level hospital. There was a collateral history of four days of progressive shortness of breath associated with an intermittent non-productive cough. He had been receiving antiretroviral therapy in the fixed-dose combination of tenofovir/ emtricitabine/efavirenz for an unspecified duration. He was restless and confused with cold, clammy peripheries. He hadKussmaul’s breathingwith a respiratory rate of 40 breaths/ min, pulse 104 beats/min and blood pressure 86/40 mmHg. The arterial blood gas revealed a severe lactic acidosis: pH 7.037, PaCO2 12.7 mmHg, PaO2 211 mmHg, serum bicarbonate 7.2 mmol/l, base deficit 27.2 mmol/l and lactate 20 mmol/l. Physical examination revealed bilateral basal crackles with no other evidence of cardiac failure. Apart from the confused state, the neurological examination was unremarkable. The patient required urgent resuscitation with intravenous fluids and a dose of ceftriaxone was administered based on a presumed diagnosis of severe sepsis/hypotension from an underlyingHIV-related pneumonia that resulted in lactic acidosis. The blood pressure did not respond to volume expansion and shortly after arrival he was placed on inotropic support with an adrenaline infusion. The patient also required intubation for increased work of breathing and potential respiratory fatigue. Despite stabilisation of his blood pressure with inotropes and maintained oxygen saturations, the acidosis continued to worsen in the ensuing eight to 10 hours. A12-leadECGshowed sinus rhythmand ST-segment depression in leads V4–V6. A POCUS examination revealed normal cardiac chamber sizes with good contractility, and a non-collapsible inferior vena cava with no pericardial or pleural effusions was noted. Blood results revealed the following: white cell count 13.58 × 109 cells/l, C-reactive protein 6 mg/l, alanine transaminase 163 U/l (normal 10–40 U/l), aspartate transaminase 258 U/l (normal 15–40 U/l), alkaline phosphatase 237 U/l (normal 53–128 U/l) and gamma-glutamyl transferase 642 U/l (normal < 68 U/l). The chest radiograph showed no evidence of pneumonia and in the absence of markers of sepsis, Shoshin beriberi was considered as the cause of the lactic acidosis/shock and he was given 300 mg of intravenous thiamine at 9:30. This was followed by a dramatic improvement in lactate levels and rapid resolution of acidosis (Table 1). Repeat blood gas three hours after thiamine admission showed the following: pH 7.24, bicarbonate 17.3 mmol/l and lactate 5.3 mmol/l. Adrenalin infusion was weaned off and he was extubated at 13:27. His blood gases continued to improve as well as the derangements in liver enzymes. Upon recovery, he admitted to drinking four jugs of homebrewed Zulu beer daily for six days a week. Repeat ECGs on discharge showed widespread T-wave inversion. Discussion These two cases typify the presentation of acute pernicious beriberi (Shoshin), which is characterised by severe lactic acidosis with circulatory shock secondary to severe thiamine deficiency.2 Thiamine deficiency leads to decreased activity of pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, both important enzymes in aerobic metabolism. There is subsequent accumulation of pyruvate and lactate in the tissues, resulting in lactic acidosis with peripheral vasodilatation and cardiac dysfunction.2,3 The Shoshin type is an uncommon form of beriberi due to advanced thiamine deficiency, which contrasts markedly with the classic presentation of high-output cardiac failure with features of a hyperdynamic circulation.1 Shoshin beriberi was first reported in early studies in the Far East secondary to chronic malnutrition and excessive consumption of polished, refined rice and cereals.3 In the Western world, Shoshin beriberi has been described mainly in alcoholics and in the critical-care setting in patients receiving total parenteral nutrition without adequate vitamin supplementation.2-4 Upon recovery both our patients admitted to excessive consumption of alcohol in the form of Zulu beer, which was probably home brewed in the light of the current restrictions on alcohol sales during the COVID-19 pandemic. Home brewed Zulu beer is usually made with fermented maize, which may contain thiaminases that remove thiamine in the brew.5 Clinical markers of excessive alcohol intake were present in both patients and included parotidomegaly, raised mean corpuscular volume and elevated gamma-glutamyl transferases.
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