This is a 56-year-old female patient with a history of active smoking, non-insulin-required type 2 diabetes mellitus (NIR DM2) and hypertension (HTN), treated with losartan 50 mg / alcohol daily
He came to the emergency service with a two-day history of compromised general condition, generalized myalgias and decreased appetite without the use of usual medications.
One day before admission, nausea and vomiting were added, which were partially managed with ondansetron, and 46dl professed diarrhoea with pathological elements, associated with capillary glucose of 50 mg/dl (10% capillary glucose control).
On physical examination at admission, the patient was wet, with no clinical signs of hypoperfusion, and with significant diffuse abdominal pain in the four quadrants, with no signs of peritoneal irritation.
Abdominal ultrasound showed no intra-abdominal injury that would explain the clinical picture.
Laboratory tests showed a high lactic acid of 173 mg/dL (VN 6.3-18.9 mg/dL) associated with a creatinine of 5.8 mg/kalemia (VN 0.5-0.9 mg/dL nitrogen plus 3.3 mg/dL).
Abdominal pain did not respond to pharmacological treatment and in parallel the patient presented deterioration of the level of consciousness, so it was decided to perform orotracheal intubation.
Computed tomography (CT) of the brain showed no acute lesions that could explain the compromise of consciousness, only microangiopathy, and CT angiography of the abdomen and pelvis showed diffuse nonspecific colitis, without signs of venous or arterial thrombosis.
Upon admission to the intensive care unit (NICU), the patient was found to be hypertensive, well perfused, but under the effects of sedation and neuromuscular blockade after intubation.
A rapid panel of arterial blood gases (AGB) was requested, which initially showed pH outside the range and after 6.8 (VN: 7.35-7.45), which was confirmed by an emergency laboratory.
In addition, polymerase chain reaction (PCR) was requested for fungal pathogens that tested positive for enteropathogenic and enteroaggregative E. coli, and antibiotic treatment with ceftriaxone and metronidazole was initiated.
Anion gap of 38 and osmolar gap of 25 stood out, so the diagnosis of metabolic acidosis with high anion gap was raised, secondary to the accumulation of lactic acid probably due to the use of metformin.
Salicylate levels were measured, which were outside the toxic range.
The patient presented hemodynamic deterioration, maintaining adequate clinical perfusion, with central venous saturation above 65% and venous-arterial CO2 difference of 5 mmHg, but with noradrenaline requirements up to 0.35 mcg/kg/h mean arterial pressure of 60 mmHg
Treatment was initiated with 500 ml of bicarbonate at 2/3 Molar in 2 h achieving a pH of 7.1 and then with high volume hemostasis (HFAV), achieving normalization of pH (7.4) and hemodynamic situation.
The next day, her clinical condition improved rapidly, being able to extubate, suspend vasoactive drugs and HVHF.
