Clinical Case 131 year old man with a history of epilepsy has a grand mal seizure. Laboratory tests taken immediately after the seizure has stopped showed:pH7.19(7.35-7.45)pCO26.10 kPa (4.5-6.0)Na+140 mmol/L(135-145)K+4.0 mmol/L(3.5-5.3)Cl-98 mmol/L(95-105)HCO3-17 mmol/L(22-30) What is the acid base disturbance? Does the patient need NaHCO3? What will happen to his potassium as the acidaemia is

corrected?

*This patient is severely ACIDAEMIC and the cause is a mixed metabolic and respiratory acidosis (low HCO3 and raised pCO2). This is a consequence of the rapid and repeated muscle contractions seen in a generalised seizure, skeletal muscle energy consumption exceeds supply (from perfusion by oxygenated blood. There may also be inadequate pulmonary gas exchange during a seizure due to poor ventilation.This rapidly reverses when the seizure activity ceases (assuming no other complicating illness) therefore no treatment is needed. Other biochemical abnormalities seen include raised potassium, raised CK, AST and sometimes ALT, released from skeletal muscle. Potassium will rapidly correct due to redistribution acroos cell membranes and enzyme levels decline according to their half life in blood.

Clinical Case 267 year old man with a previous diagnosis of liver cirrhosis. Admitted because of haematemesis and melaena. He took occasional antacids but was on no other prescribed medication. On examination, he was very ill, short of breath, pulse 120 beats per minute, blood pressure 60/40 mmHg.Na139 mmol/L(135-145)K4.8 mmol/L(3.5-5.3)Cl98 mmol/L(95-105)HCO37 mmol/L(22-30)Urea24.0 mmol/L(2.5-7.5)Creatinine240 mol/L(60-120)pH7.13(7.35-7.45)pCO22.93 kPa (4.5-6.0)Glucose6.6 mmol/LHaemoglobin55 g/L(130-180)Lactate28mmol/l(

Clinical Case 3A 35 year old female had a history of small bowel resection due to a mesenteric thrombosis.Na139 mmol/L(135-145)K2.7 mmol/L(3.5-5.3)Cl114 mmol/L(95-105)HCO38 mmol/L(22-30)Urea3.1 mmol/L(2.5-7.5)Creatinine58 mol/L(60-120)

Comment on the electrolytes What additional tests should be done?

*Patients who have had extensive bowel resections are at risk of complications collectively known as short bowel syndrome. These include malabsorbtion and bacterial overgrowth. This patient has a low potassium (which may indicate GI losses) in association with a high anion gap metabolic acidosis. Ketones were negative. L-lactate was 1.0 mmol/l but special assay of D-lactate was 3.0 mmol/l (normally undetectable). Urine D-lactate was 43 mmol/l. D-lactic acidosis is usually seen where there has been jejuno-ileal bypass or extensive resection of small bowel. The colon receives an abnormal load of carbohydrate and sugars and there is also an alteration in the normal bowel flora favouring gram positive anaerobes which metabolise starch and sugars to D-lactate. Patients typically get episodic metabolic acidosis associated with neurological symptoms including confusion, cerebellar ataxia, slurred speech and loss of memory. Their symptoms may be quite clearly linked to taking high carbohydrate meals. They may complain of feeling drunk after meals even though they have taken no alcohol. The usual assays for lactate only recognise the normal L isomer. Also, D-lactate is rapidly filtered in the kidney and in contrast to L-lactate is POORLY reabsorbed.

*This patient is severely ACIDAEMIC and the cause is a mixed metabolic and respiratory acidosis (low HCO3 and raised pCO2). This is a consequence of the rapid and repeated muscle contractions seen in a generalised seizure, skeletal muscle energy consumption exceeds supply (from perfusion by oxygenated blood. There may also be inadequate pulmonary gas exchange during a seizure due to poor ventilation.This rapidly reverses when the seizure activity ceases (assuming no other complicating illness) therefore no treatment is needed. Other biochemical abnormalities seen include raised potassium, raised CK, AST and sometimes ALT, released from skeletal muscle. Potassium will rapidly correct due to redistribution acroos cell membranes and enzyme levels decline according to their half life in blood. *This patient has a severe HAGMA due to a combination of Shock and anaemia (leading to Type A lactic acidosis) on a background of cirrhosis and possible chronic renal impairment (Type B lactic acidosis). Note: urea may be raised due to GI bleeding and absorbtion of excess nitrogenous breakdown products. The renal impairment may be pre-renal due to hypovolaemia and poor perfusion. Liver and kidney are key organs for gluconeogenesis. However glycogen stores are likely to be poor in a patient with cirrhosis (poor nutrition is common) and gluconeogenic enzymes function poorly if oxygen supply is compromised. This leads to a vicious circle of lactate over-production and poor clearance. *Patients who have had extensive bowel resections are at risk of complications collectively known as short bowel syndrome. These include malabsorbtion and bacterial overgrowth. This patient has a low potassium (which may indicate GI losses) in association with a high anion gap metabolic acidosis. Ketones were negative. L-lactate was 1.0 mmol/l but special assay of D-lactate was 3.0 mmol/l (normally undetectable). Urine D-lactate was 43 mmol/l. D-lactic acidosis is usually seen where there has been jejuno-ileal bypass or extensive resection of small bowel. The colon receives an abnormal load of carbohydrate and sugars and there is also an alteration in the normal bowel flora favouring gram positive anaerobes which metabolise starch and sugars to D-lactate. Patients typically get episodic metabolic acidosis associated with neurological symptoms including confusion, cerebellar ataxia, slurred speech and loss of memory. Their symptoms may be quite clearly linked to taking high carbohydrate meals. They may complain of feeling drunk after meals even though they have taken no alcohol. The usual assays for lactate only recognise the normal L isomer. Also, D-lactate is rapidly filtered in the kidney and in contrast to L-lactate is POORLY reabsorbed.