This is a 43-year-old woman with a history of headache and generalized tonic-clonic seizures of recent onset.
Due to its symptomatology, a perirrolándica (Spetzler III), dependent on the right middle cerebral artery, was diagnosed and studied.
Given the characteristics of the lesion it was decided to perform surgical treatment.
The patient received anticonvulsant treatment with valproic acid because she was allergic to phenytoin.
On June 13, 2006, at 08:00, the patient underwent right parietal craniotomy and AVM resection.
During the 7 hours of the surgical procedure, 7mg/kg/h (117 mg/kg/min) propofol and 0.25 mg/kg/min remifentanil were administered.
AVM exeresis could be successfully performed without intraoperative complications.
In the immediate postoperative period (still in the pavilion), the patient presented a generalized tonic-clonic seizures that resolved with 4 mg of lorazepam intravenously.
At 16:00 p.m. on the same day and once admitted fentanyl, the patient was admitted to the Intensive Care Unit (ICU) with valvulanic acid and maintained under mechanical ventilation. Neuroprogesic acid control was continued.
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Blood chemistry tests were within normal ranges, with no renal, hepatic or coagulation dysfunction and no evidence of active infection.
However, at 17:00 there was evidence of incipient lactic acidosis with pH 7.34; PaC02 36 mmHg, Bicarbonate 19 mmol/L; diuresis BE - 6.4 mmol/L and transient lon cardiac acid 4.1 mmol/L.
After initial stabilization, a control brain CT was performed, showing post-surgical changes: surgical bed without hematoma and preserved midline.
The electroencephalogram ruled out the existence of epileptogenic activity and showed a generalized slow rhythm attributable to sedation.
Standard postoperative management measures were maintained, ensuring adequate cerebral perfusion pressure.
During the following hours the patient did not present new motor seizures.
At 21:00 hours, a new gastrointestinal control highlights the worsening of lactic acidosis: pH 7.12; PaC02 31 mmHg; bicarbonate 10 mmol/L; BE-18 mmol/L with 86% central venous acid.
The electrocardiogram showed no changes suggestive of myocardial ischemia and cardiac enzymes were normal.
In this context, it was decided to perform invasive haemodynamic monitoring with a pulmonary artery catheter, finding an Occlusion pressure in the pulmonary artery (POAP) of 10 mmHg, a mixed venous resistance index of 5.2 m/f
Fluid intake was continued with a target PAOP of 14 to 16 mmHg and noradrenaline was added to maintain a MAP of 90 to 100 mmHg.
Additionally, midazolam infusion was increased to 20 mg/h and propofol administration was restarted at 3.5 mg/kg/h (58 Lig/kg/min) to reach a level of 2kergation on the sedation-sedation scale.
However, despite remaining stable in the macro- and micro-hemodinomic areas and without organic dysfunctions, in the control of 00:20, worsening of lactic acid S8.5 80% was strikingly observed with pH 8.5.
It was not possible to identify an evident cause that explained the clinical evolution of the patient, support therapy was maintained.
In the following hours, no significant change in metabolic acidosis was observed.
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Finally, it was stressed that propofol administration could be the triggering and perpetuating cause of lactic acidosis, so it was decided to stop the infusion at 08:30, having completed 8 additional hours after surgery
The hemodynamic condition remained stable during the morning.
Four hours later a new blood gas control was performed, which showed correction of lactic acidosis: pH 7.53 and lactic acid 2.9 mmol/ L with PaC02 24 mmHg.
At 19:00, eleven hours after propofol withdrawal, lactic acid was already present: 1.6/L. Subsequently, the patient had a favorable evolution without complications associated with normalized metabolic syndrome.
She did not present seizures again and could be extubated and discharged from the ICU in good condition.
