ABG interpretationABG interpretationcase scenariocase scenario

Kamal Osman MerganiKamal Osman Mergani

Consultant intensivistConsultant intensivist

Case presentationCase presentation

15 Y/O male patient underwent 15 Y/O male patient underwent craniotomy and resection of a fronto-craniotomy and resection of a fronto-temporal tumor. temporal tumor.

After around 5 hours uneventful surgery, After around 5 hours uneventful surgery, he was extubated and transferred to ICU. he was extubated and transferred to ICU. He was conscious with GA residual He was conscious with GA residual effects, hemodynamically stable, effects, hemodynamically stable, spontaneously breathing on O2 8 LPM spontaneously breathing on O2 8 LPM via face mask with good urine outputvia face mask with good urine output

ABGABG

Initial ABG showed the following Initial ABG showed the following results: results: pH: 7.22pH: 7.22pCO2: 36.7pCO2: 36.7pO2: 181.5pO2: 181.5HCO3-: 14.7HCO3-: 14.7SaO2: 99.6%SaO2: 99.6%

ABGABG

Na: 141Na: 141K: 3.9K: 3.9Cl: 104Cl: 104Ca++: 1.15Ca++: 1.15Hb: 127Hb: 127Lactate: 7.8Lactate: 7.8

• What is your impression What is your impression and management and management ?? ??

ABG analalysisABG analalysis

pH of 7.22 and HCO3 of 14.7 indicating pH of 7.22 and HCO3 of 14.7 indicating metabolic academia.metabolic academia.

Predicted Predicted PCO2PCO2 (Respiratory compensation): (Respiratory compensation): PCO2= 1.5 X[HCO3]+8PCO2= 1.5 X[HCO3]+8

therefore PCO2 should have beentherefore PCO2 should have been

1.5X14.7+8= 30 1.5X14.7+8= 30

but actual is but actual is 36.736.7 indicating combined indicating combined respiratory respiratory and metabolic acidosisand metabolic acidosis

ABG analalysisABG analalysis

AG= Na-(Cl+HCO3)= 141-(104+15)= 22AG= Na-(Cl+HCO3)= 141-(104+15)= 22∆ AG= 22-12= 10∆ AG= 22-12= 10∆ HCO3= 24-15= 9∆ HCO3= 24-15= 9Thus ∆ HCO3 = ∆ AG Thus ∆ HCO3 = ∆ AG indicating no indicating no combined combined non-anion gap non-anion gap metabolic metabolic acidosis acidosis

Added anions= 10 mmol/L= 8 Lactic acid + Added anions= 10 mmol/L= 8 Lactic acid + 2 ? 2 ?

ABG analalysisABG analalysis

Final diagnosis combined Final diagnosis combined metabolic lactic metabolic lactic acidosis acidosis indicating hypoperfusion and indicating hypoperfusion and respiratory acidosis respiratory acidosis indicating respiratory indicating respiratory suppression secondary to residual general suppression secondary to residual general anesthesia effects.anesthesia effects.

HR was around 100↑ and CVP around 5↓HR was around 100↑ and CVP around 5↓

F/U of patientF/U of patient

As the patient is more awake now and with As the patient is more awake now and with the resolution of general anesthesia the resolution of general anesthesia effects, it is clear that the patient now has effects, it is clear that the patient now has metabolic acidosis metabolic acidosis with full respiratory with full respiratory compensation secondary to compensation secondary to lactic acidosislactic acidosis

Lactic acidosisLactic acidosis

The most frequent cause of The most frequent cause of lactic acidosis lactic acidosis is is type A type A that is secondary to poor tissue that is secondary to poor tissue perfusion, which is induced by various perfusion, which is induced by various shock states causing tissue hypoxia, but shock states causing tissue hypoxia, but you are ruling out any hypotension in the you are ruling out any hypotension in the peri-operative period!peri-operative period!

Type B1Type B1, has been identified with diabetes , has been identified with diabetes mellitus, bowel ischemia, severe iron-mellitus, bowel ischemia, severe iron-deficiency anemia, liver disease, alcoholic deficiency anemia, liver disease, alcoholic ketoacidosis, pancreatitis, malignancy ketoacidosis, pancreatitis, malignancy (leukemia, lymphoma, lung cancer), (leukemia, lymphoma, lung cancer), infection, renal failure, seizures, heat infection, renal failure, seizures, heat stroke, pheochromocytoma, thiamine stroke, pheochromocytoma, thiamine deficiency, short gut syndrome, and other deficiency, short gut syndrome, and other carbohydrate malabsorption syndromescarbohydrate malabsorption syndromes

Type B2 lactic acidosisType B2 lactic acidosis

Medicinal and toxic causes of lactic Medicinal and toxic causes of lactic acidosis, known as acidosis, known as type B2type B2, are , are numerous, including acetaminophen, numerous, including acetaminophen, alcohols and glycols (ethanol, ethylene alcohols and glycols (ethanol, ethylene glycol, methanol, propylene glycol), glycol, methanol, propylene glycol), antiretroviral nucleoside analogs antiretroviral nucleoside analogs (zidovudine, didanosine, ...lamivudine), (zidovudine, didanosine, ...lamivudine),

Type B2 lactic acidosis Type B2 lactic acidosis

Beta-adrenergic agents (epinephrine, ritodrine, Beta-adrenergic agents (epinephrine, ritodrine, terbutaline), biguanides (phenformin, metformin), terbutaline), biguanides (phenformin, metformin), cocaine, cyanogenic compounds (cyanide, cocaine, cyanogenic compounds (cyanide, aliphatic nitriles, nitroprusside), diethyl ether, 5-aliphatic nitriles, nitroprusside), diethyl ether, 5-fluorouracil, halothane, iron, isoniazid, propofol, fluorouracil, halothane, iron, isoniazid, propofol, sugars and sugar alcohols (fructose, sorbitol, sugars and sugar alcohols (fructose, sorbitol, and xylitol), salicylates, strychnine, and xylitol), salicylates, strychnine, sulfasalazine, and valproic acid. sulfasalazine, and valproic acid.

Type B3 lactic acidosis Type B3 lactic acidosis

B3 lactic acidosis may result in those with B3 lactic acidosis may result in those with inborn errors of metabolism. These include inborn errors of metabolism. These include glucose-6-phosphatase deficiency (von glucose-6-phosphatase deficiency (von Gierke disease), fructose-1,6-Gierke disease), fructose-1,6-diphosphatase deficiency, pyruvate diphosphatase deficiency, pyruvate carboxylase deficiency, pyruvate carboxylase deficiency, pyruvate dehydrogenase deficiency, oxidative dehydrogenase deficiency, oxidative phosphorylation deficiency, and phosphorylation deficiency, and methylmalonic aciduriamethylmalonic aciduria

Lactic acidosis rarely may present in the Lactic acidosis rarely may present in the MELAS syndrome (mitochondrial MELAS syndrome (mitochondrial encephalopathy, lactic acidosis, and stroke encephalopathy, lactic acidosis, and stroke like episodes), which appears to be caused like episodes), which appears to be caused by a point mutation in mitochondrial DNA by a point mutation in mitochondrial DNA tRNALeu (UUR) gene. This syndrome is tRNALeu (UUR) gene. This syndrome is characterized by migraine like headaches, characterized by migraine like headaches, dementia, hearing loss, ataxia, and dementia, hearing loss, ataxia, and episodic vomiting.episodic vomiting.

Back to the patientBack to the patient

Patient was managed with NS boluses of Patient was managed with NS boluses of total 1.5 L since the admission to ICU. total 1.5 L since the admission to ICU.

The lactate level dropped to 4.3 after 4 The lactate level dropped to 4.3 after 4 hours of the last ABG then to 0.8 after 12 hours of the last ABG then to 0.8 after 12 hours of ICU admission. hours of ICU admission.

This will rule out type B1 and the toxic This will rule out type B1 and the toxic (medical) causes(medical) causes

The explanation was possible hypothermia The explanation was possible hypothermia during the anesthesia which is common in during the anesthesia which is common in the neurosurgical procedures (and may be the neurosurgical procedures (and may be severe shivering during the recovery). The severe shivering during the recovery). The lactate level will start to increase during lactate level will start to increase during the warming periods and continues for the warming periods and continues for hours before starting clearance. Probably hours before starting clearance. Probably there is some metabolic disorder as well there is some metabolic disorder as well made it so severe. made it so severe.