NEPHROLOGY, DIALYSIS AND TRANSPLANTATION CASE STUDIES

 

A 75-year-old woman, body weight: 72 kg, length: 167 cm, is known with type II diabetes mellitus since more than 20 years, and has all the typical features of this disease (retinopathy, neuropathy, nephropathy, macroangiopathy, microangiopathy, and hypertension). Renal problems are known since 1990, somewhat later she became wheelchair-bound due to polyneuropathy, in 1992 she underwent an amputation of the left big toe, in 1995 hemodialysis was started, and in 1995 and 1999 she underwent plastic surgery of the skin of the legs because of necrosis. She is anuric since 1997. Attempts to create an elbow AV-fistula failed, so that she is dialysed since many years on a soft tunnelled indwelling central venous catheter in the deep jugular vein (type TesioR), in a single needle mode.
On 25/05/00 she is admitted to the Hospital with a clinical picture of sepsis, combined with mental confusion and severe constipation. Fever reaches up to 39.2° C in combination with chills. Three consecutive blood cultures reveal Staphylococcus aureus, methicillin sensitive. Leukocyte counts rise up to 13,885 cells/mm3 and CRP to 18.1 mg/L. Most other admission laboratory features were normal.
As it was impossible to identify any alternative focus, a temptative diagnosis of "catheter sepsis" was put forward.
Treatment was started with Na-oxacillin (PenstaphoR) I.V., at a dose of 4x1g/D for 1 week, followed by a switch to peroral, which however induced gastro-intestinal complaints, so the patient was further treated with Vancomycin (VancocinR) I.V. (3 weeks). The antibiotic treatment decreased CRP consistently since its start and CRP normalised after one week.
Apart from the laboratory features mentioned above, the most striking and unexpected biochemical abnormality upon admission was, however, a hypokalaemia of 2.2 mmol/L.

QUESTIONS 1 AND 2

Study of routine potassium determinations over the last months, revealed a progressive decline of potassaemia, in absence of changes of dialysate potassium (2 mmol/L), but a pathologically low value had been observed only once, 3 days before the hospital admission. Blood had been sampled each time pre-dialysis:
18
18/02/00 5.0 mmol/L
18/03/00 4.5 mmol/L
25/04/00 3.9 mmol/L
03/05/00 3.5 mmol/L
20/05/00 2.7 mmol/L
25/05/00 2.2 mmol/L

 

QUESTIONS 3, 4 AND 5

Clinically, a progressively distending abdomen was registered, together with clangourous bowel sounds upon auscultation.

 

QUESTION 6

The technical investigations gave the following results:

Plain X-ray of the abdomen:

 

Gastrographine clysma of the colon:

CT-scan of the abdomen: Also this investigation confirmed the extreme distension, without objectivation of a specific obstructive lesion.

Colonoscopy: Only revealed a localised ischemic zone with diffuse bleeding spots, corresponding to ischaemia.

 

QUESTIONS 7 AND 8

In this case, the potassium was administered intravenously, and potassium was increased in the dialysate to 4 mmol/L. After one week of IV repletion, the patient was switched to peroral potassium. The gain in serum potassium was deceiving, however.

18/06/00 2.7 mmol/L
23/06/00 2.8 mmol/L (last administration of antibiotic)
15/07/00 2.3 mmol/L

The abdomen remained distended. At this moment, it was decided to switch to daily dialysis:

08/08/00 2.8 mmol/L
11/08/00 3.7 mmol/L
17/08/00 3.8 mmol/L

At a routine control of CRP, again a sudden rise to 18.0 mg/dL was found, without a febrile episode nor complaints of shivering; blindly collected haemocultures (3 times) were all negative . Abdominal distension had in the meanwhile increased further up to dramatic proportions. Caecal diameter on plain abdomen X-ray largely exceeded 11 cm. Teicoplanin (TargocidR) was started, however without major effect on CRP (14.7 mg/dL after 1 week).

 

QUESTIONS 9 AND 10

Further evolution and summary:

A colonostomy was installed on 06/09/00. Pre-dialysis potassium, which still was 2.8 mmol/L on 08/08/02, gradually rose to 3.5 (22/09/00), and 3.9 mmol/L (26/09/00). It was 4.0 mmol/L on 01/08/01 while dialysate potassium had been lowered to 1.0 mmol/L. As of today, the patient still has the colonostomy, and radiological check-ups revealed that intestinal distension, and signs of gas and fluid accumulation have completely disappeared.

The present case illustrates a problem of hypokalaemia in a dialysed patient with diabetes mellitus. Although the primary episode of abdominal distension and hypokalaemia might have been induced by a catheter sepsis, the problems persisted, even after adequate treatment of both sepsis and hypokalaemia. Subsequently, intestinal distension as a consequence of diabetic neuropathy was held responsible. After an initial unsuccessful attempt of treatment with repeated colonoscopies, and in view of the gravity of the condition, a colonostomy was installed, after which intestinal distension and hypokalaemia disappeared.

Acknowledgements: The author is indebted to A Dhondt, and H Van Vlierberghe for revising the manuscript and giving useful suggestions.