VNJ Volume 39 (3) June 2024 | Page 43

Plus-Hex CLINICAL
Urethral obstruction
Feline UO is a common complication in patients with feline lower urinary tract disease ( FLUTD ) and can develop due to urolithiasis , urethral plugs , idiopathic obstructions or , in rare cases , strictures or neoplasia [ 2 ] . UO causes urine to return to the kidneys , due to increased intravesical pressure and distension of the urinary bladder , which results in increased intratubular pressure and a decreased glomerular filtration rate [ 3 ] . This affects tubular concentrating capacity , particularly reabsorption , K + excretion and water / sodium regulation , resulting in uraemia , hyperkalaemia and acidosis , which left untreated can be fatal [ 4 ] . Neutered male cats are over-represented among UO patients ; this is thought to be due to their urethra being longer and narrower than in female cats [ 5 ] . Environmental factors , stress , obesity , diet and urine pH can contribute to the underlying cause of FLUTD . The long-term prognosis for patients with UO is guarded , due to the high risk of recurrence of an obstruction and the associated clinical signs , and euthanasia is a common outcome [ 6 ] .
Metabolic acidosis
Normal tissue function is maintained within a narrow range of concentration of free hydrogen ions ( H + ) that are not bound to any other molecule . This concentration is represented by the pH , and is regulated by the kidneys [ 7 ] . The kidneys excrete the normal acid load generated by protein metabolism . Therefore , renal impairment – such as that seen in UO – will result in acidic by-products remaining in the body , which will cause an acid – base imbalance called metabolic acidosis [ 8 ] . Left untreated , metabolic acidosis can cause arterial vasodilation , decreased myocardial contractility , coagulopathies , insulin resistance , altered central nervous function and decreased renal and hepatic blood flow [ 9 ] .
By taking a baseline sample from the patient on admission , the severity of the metabolic acidosis can be identified and a treatment plan tailored to the patient ' s needs [ 7 ] . Acid – base imbalances are usually corrected once the underlying cause has been treated and suitable fluid therapy has been administered [ 8 ] .
Because this patient ' s urine collection system had been clamped , the urine flow was obstructed , so the metabolic acidosis could not correct itself . Unfortunately , the PCP had not carried out blood gas analysis , so it could not be determined whether the acidosis had altered since the patient ' s initial presentation . However , it can be presumed that the acidosis had worsened , as the patient arrived on saline fluids , which are acidifying . They contain no buffer , which could potentially have contributed to the near-fatal pH of the patient on admission to the OOH service , as a pH of < 6.85 is not compatible with life [ 8 ] .
Buffers are molecules that play an important role in regulating the pH in the body by binding to H + . The bicarbonate buffer system is the most important system in the blood [ 8 ] . Bicarbonate neutralises acid produced by metabolic processes , and carbonic acid neutralises bases produced by protein breakdown , such as urea [ 10 ] . The reversible equation shown below demonstrates the essential relationship between carbon dioxide ( CO 2
) and bicarbonate ( HCO 3
), which allows appropriate blood and tissue metabolic function by maintaining pH within a narrow margin [ 11 ] .
CO 2
+ H 2 O ↔ H 2
CO 3
↔ H + + HCO 3
The concentration of CO 2 is regulated by the lungs and the HCO 3
– concentration is regulated by the kidneys . The bicarbonate buffer system is an open system [ 11 ] . This physiological regulation means that there is minimal disruption of pH to maintain normal tissue function and metabolism [ 7 ] . However , when tissues become ischaemic , they function as a closed system with no connection to the lungs to remove CO 2
, resulting in a larger change in pH [ 8 ] . In UO , the tissue of the urinary tract can become ischaemic due to poor blood flow to the area , causing anaerobic metabolism , resulting in the production of lactic acid , which contributes to metabolic acidosis [ 7 ] . This patient had a normal blood lactate concentration on presentation to the OOH service ; the metabolic acidosis was likely to have been due to the physical obstruction to urine output , with the liver compensating appropriately for hyperlactataemia , making lactate appear normal .
In metabolic acidosis , the increase in H + causes a shift to the left in the bicarbonate buffer system equation , with an increase in CO 2 needing to be eliminated [ 8 ] . Therefore , patients with acute metabolic acidosis will typically be hyperventilating , causing a decrease in the partial pressure of carbon dioxide ( PCO 2
), emphasising the respiratory compensation [ 7 ] . In this case , the patient had a PCO 2 of 40.3 mmHg ( the normal range for cats is 32.7 – 44.7 mmHg ), which indicates that its respiratory system was not compensating for the metabolic acidosis .
Restoration of the acid – base imbalance to normal can be achieved by restoring the depleted HCO 3
– with sodium bicarbonate ( NaHCO 3 ) [ 3 ] . HCO 3
– can also help in the excretion of urea by combining with ammonium cations ( NH 4
+
) to produce ammonia ( NH 3 )
( NH 4
HCO 3
→ NH 3 + CO 2
+ H 2
O ), which is excreted via the proximal convoluted tubule [ 3 ] . Theoretically , the administration of NaHCO 3 in cases of metabolic acidosis has an alkalinising effect , as it binds to the excessive H + to form carbonic acid , which rapidly dissociates into CO 2 and water [ 8 ] . In cases where it is considered appropriate , NaHCO 3 can be administered at 1 – 4 mEq / kg over 10 min [ 12 ] . If there is no respiratory compensation ( hyperventilating ) in response to the increase in CO 2
, it will combine with water to produce carbonic acid again , further decreasing the pH [ 3 ] . Therefore , in this patient , NaHCO 3 would be contraindicated , as it had already been found that the patient had no respiratory compensation for its metabolic acidosis .
Volume 39 ( 3 ) • June 2024
43