Ostroski CJ, Cooper ES. Development of dialysis disequilibrium-like clinical signs during postobstructive management of feline urethral obstruction. J Vet Emerg Crit Care 2014. 24(4):444-449.
Tomcat urethral obstruction is one of my favourite topics to discuss and teach about (sad, I know!) and yet again they do not fail me! Like many of you I’m sure, I have managed a large number of tomcats with urethral obstruction in my time and I don’t recall this progression ever happening. I have been aware of dialysis disequilibrium syndrome, especially having worked in a hospital where dialysis is available, and I found this case report very interesting. As always of course it is very difficult to know the true incidence of this development in blocked tomcats as it may go unrecognised by the people managing the case if neurological signs are attributed to another aetiology, or indeed it may be suspected but go unreported. I guess I can say that from my own personal experience and that of colleagues, it is a rare development in tomcats with urethral obstruction but definitely something to bear in mind.
Have you ever come across this before? If so, I would love to hear about it!
Case report highlights
Some of the bits from the report that I thought it worth including here are as follows. If anyone actually wants a PDF of the case report then feel free to email me – I think it is okay for me to send a copy to individuals for educational purposes without breaking any laws!
“Dialysis disequilibrium syndrome (DDS) is characterized by neurologic symptoms of varying severity resulting from overly rapid decreases in peripheral osmolality during a dialysis procedure…With rapid decreases in blood osmolality, cerebral edema develops due to the resulting gradient between cerebral tissues and blood, causing an acute increase in intracranial pressure. This syndrome has been recognized in both human and veterinary patients undergoing hemodialysis…Cats with urethral obstruction are often severely azotemic on presentation and therefore have the potential for similar rapid decreases in urea concentrations in the postobstructive period. The purpose of this report is to describe an instance of suspected postobstructive DDS-like clinical signs in a male cat.”
This was a 5-year old castrated male domestic short hair cat weighing 5.26 kg.
On presentation this patient was towards the severe end of the spectrum of presentation being moribund and with clinically significant hyperkalaemia; interestingly also a mild hypoglycaemia (not unheard of in these cases but I would say definitely unusual) that actually persisted and had to be corrected by supplementation.
Nothing about the management was especially noteworthy I would say (cystocentesis was performed before catheterisation was attempted which is very much not what I do/teach but let’s leave that aside on this occasion!).
Following catheterisation the cat developed a marked post-obstructive diuresis.
Approximately 5 hours after catheterisation he had a generalised seizure and then developed respiratory arrest:
“Repeat assessment of electrolyte concentrations and blood-gas values revealed resolution of acidemia, mild hypocalcemia, and marked reduction in azotemia…Given that neither hypoglycemia nor hypocalcemia appeared to be the cause of the seizure activity, the concern was raised that an acute change in BUN, and thereby osmolality was responsible (in a process similar to DDS). Because of this concern, the patient was administered a bolus of 7% hypertonic saline (2 mL/kg, IV) over 5 minutes. By the end of the infusion he started to breathe spontaneously and his PLRs had improved. The patient was still mentally obtunded but was able to be extubated 15 minutes later….Approximately 90 minutes after this initial episode, the cat's neurologic condition again deteriorated. He displayed opisthotonus and his PLRs were diminished. Because of the continued concern for osmotic injury, the patient was given an additional IV bolus of hypertonic saline (2 mL/kg), after which the cat's mentation again improved. At this point, a continuous rate IV infusion of 3% sodium chloride was initiated in an effort to maintain blood osmolality and to prevent further clinical signs….The following morning, the patient's mentation remained depressed but he was slightly more responsive; there were no further seizures….His mental status steadily improved throughout the course of the day and his urine output (and IV fluid rate) gradually decreased.
Throughout the remainder of hospitalization the patient's neurologic status continued to improve and appeared to be completely mentally appropriate within 40 hours of the onset of seizure activity.”
He was eventually discharged and was reportedly doing fine at follow up after 2 days and 3 months.
“As a clinical syndrome, DDS has been reported in human and veterinary patients undergoing hemodialysis for treatment of renal disease.
The pathogenesis of DDS is still unclear, but there are 2 major theories to explain the development of cerebral edema. Both theories are predicated on the presence of a hyperosmolar state and the development of a gradient between cerebral tissues and the blood followed by rapid reduction of peripheral osmolality. The result is an intracellular shift of extracellular water leading to neuronal swelling, increased intracranial pressure, and the clinical signs associated with cerebral edema (eg, dull mentation, seizures).” I am not going to include any more detail about the theories here!
“The diagnosis of DDS is one of exclusion, and is primarily based on a predisposing clinical situation and development of characteristic neurologic signs…DDS has been documented in both experimental models and clinical reports of veterinary species undergoing dialysis…Based on clinical signs and available laboratory data, we suspect that the patient described in this report suffered from clinical signs similar to DDS. This syndrome is typically seen in patients that undergo a rapid decrease in serum urea in a short period and is a diagnosis of exclusion. In this case, the patient had BUN of 89.3 mmol/L [250 mg/dL] at first measurement that rapidly decreased to 19.9 mmol/L [56 mg/dL] over a 7 hour time span. This likely occurred secondary to a marked post-obstructive diuresis, producing 92.5 mL/h of urine in the 4 hours just prior to the onset of neurologic signs. Although the decline of BUN is not as rapid as that seen with DDS in hemodialysis patients, this patient still experienced a change in osmolality of 67 mOsm/kg (or ∼ 9 mOsm/kg/h) during that period, much faster than the target rate of 1–2 mOsm/kg/h...Furthermore, administration of hypertonic saline repeatedly resulted in significant improvement in the patient's neurologic status, supporting the notion that the signs were a result of changes in serum osmolality.”
“Based on the clinical signs, laboratory values, and response to treatment, we suspect that this patient experienced an episode (characterized by altered mentation, seizure, and brief cessation of breathing) consistent with the clinical syndrome associated with DDS. The patient's neurologic signs corresponded with rapid decreases in BUN (secondary to marked postobstructive diuresis) and responded to treatment with a hyperosmolar solution. To the authors’ knowledge, this has not been reported as a potential complication to treatment of feline urethral obstruction in veterinary medicine. Practitioners should be aware of this potential complication as a cause of prolonged neurologic recovery or seizures in the postobstructive period of severely azotemic patients, and frequent monitoring of electrolytes, BUN, and neurologic status may be indicated. If rapid decreases in osmolarity and BUN are detected during early case management, or if otherwise unexplained neurologic signs develop, administration of hyperosmolar solutions may be of benefit.”