Uncovering the basis of a severe degree of acidemia in a patient with diabetic ketoacidosis

Abstract

In this teaching exercise, the goal is to demonstrate how an application of principles of physiology can reveal the basis for a severe degree of acidaemia (pH 6.81, bicarbonate <3 mmol/l (P(HCO(3))), PCO(2) 8 mmHg), why it was tolerated for a long period of time, and the issues for its therapy in an 8-year-old female with diabetic ketoacidosis. The relatively low value for the anion gap in plasma (19 mEq/l) suggested that its cause was both a direct and an indirect loss of NaHCO(3). Professor McCance suggested that ileus due to hypokalaemia might cause this direct loss of NaHCO(3), and that an excessive excretion of ketoacid anions without NH(4)(+) in the urine accounted for the indirect loss of NaHCO(3). In addition, he suspected that another factor also contributing to the severity of the acidaemia was a low input of alkali. He was also able to explain why there was a 16-h delay before there was a rise in the P(HCO(3)) once therapy began. The missing links in this interesting story, including a possible basis for the hypokalaemia, emerge during the discussion between the medical team and Professor McCance.

Occult risk factor for the development of cerebral edema in children with diabetic ketoacidosis: possible role for stomach emptying

“…A major difficulty in identifying risk factors for cerebral edema is that patients with DKA represent a heterogeneous population with respect to biochemical findings on admission as reflected by the data in Table 5(20, 30). One reason for these marked differences may be the predominant dietary intake prior to admission, and also recent changes in this intake.…”

“…In addition, he has a very high P Effective Osm . In contrast, the patient on the right drank a dilute solution containing sugar, but not the K + or potential HCO − 3 in fruit juice (20). As a result, there was a much lower P Glucose , hypokalemia, and a surprisingly severe degree of metabolic acidosis.…”

“…The intake of this type of fluid instead of fruit juice should be suspected if the patient lacks evidence for a large intake of sugar (750 mmol of monosaccharides per liter), and the other constituents of fruit juice (i.e., 50 mEq/L of potassium (K + )) and organic anions [potential bicarbonate (HCO − 3 ) ], reviewed in reference (19). Thus, there will be a lower than expected P Glucose , a very low concentration of K + (P K ), HCO − 3 (P HCO3 ), and pH in plasma (i.e., a very severe degree of metabolic acidosis) (20). Patients who drank solutions with little glucose were very unlikely to be included in our retrospective chart review, as the major criterion for patient selection was a P Glucose > 900 mg/dL (50 mmol/L).…”

“…A major difficulty in identifying risk factors for cerebral edema arises from the fact that patients with DKA are not a homogenous group with respect to their biochemical values on admission. One reason for these marked differences may be whether their prior intake included a major ingestion of fruit juice or similar fluids rich in sugar, K + , and organic anions (potential HCO − 3 ) (20, 30). As illustrated in Table 5, the patient with a less severe degree of hyperglycemia also had a low P K , low P HCO3 , and a more severe degree of acidemia, which may represent a low intake of the constituents of fruit juice.…”

Effect of altitude on brain intracellular pH and inorganic phosphate levels

“…In fact, an increase or decrease in the blood concentration of free protons of as little as 0.1 µM is fatal (Richerson, 2004). An increased concentration of intracellular hydrogen ions, resulting from acidification, may bind with brain proteins, potentially altering their shape and function as enzymes, transporters, contractile elements and structural components (Gowrishankar et al, 2007). Conversely, in pathological states that induce respiratory alkalosis, hypocapnia is known to produce neuronal ischemia and injury (Laffey and Kavanagh, 2002; Curley et al, 2010).…”