Urethral Obstruction Flashcards
In what animal are urethral obstructions most common? What are the 2 types of causes?
male cats and dogs - narrow urethra
- physical - urolith, neoplasia, mucosal plug, stricture
- mechanical - urethral spasm
What is the most life-threatening disturbance seen in cases of urethral obstructions? Why does this occur? What does this lead to?
hyperkalemia
decreased renal potassium excretion and extracellular shift due to acidosis
causes cardiac myocytes to be unable to depolarize, leading to bradycardia +/- tall T waves, widened QRS complexes, and decreased to absent P waves on ECG
Other than hyperkalemia, what are 5 other metabolic changes commonly seen in cases of urethral obstruction?
- hypovolemia and cardiovascular compromise
- azotemia
- metabolic acidosis
- hypocalcemia
- hyperphosphatemia
What needs to be immediately treated in cases of urethral obstructions? What are 4 parts of the treatment plan?
hyperkalemia
- IV fluids (0.9% NaCl) - dilutional effect to lower serum potassium
- IV calcium gluconate - restores membrane potential and re-establish normal depolarization –> does NOT lower K
- IV dextrose and Regular insulin - moves potassium back into cells
- sodium bicarbonate - shifts potassium back into cells as pH increases
Can insulin be given alone as a way to treat hyperkalemia in case of urethral obstructions?
NO –> can cause hypoglycemia and seizures, give with IV dextrose!
Why does metabolic acidosis occur in cases of urethral obstructions? What does it result in? What 3 things does it predispose the patient to?
secondary to the inability of the kidneys to excrete hydrogen ion (can have a pH <7.0)
respiratory compensation –> increased RR and tidal volume
- cardiac arrhythmia
- reduced catecholamine responsiveness
- CNS depression
What are 3 ways of treating metabolic acidosis in cases of urethral obstructions?
- re-establish GFR by decompressing the bladder
- IV fluid therapy
- sodium bicarbonate - typically reserved for severe acidosis with a pH <7.1 and HCO3 <10 mmol/L
What causes azotemia and hyperphosphatemia as a result of urethral obstruction? What does it result in?
decreased renal excretion of urea and other waste products
CNS depression
What are 2 ways of treating azotemia and hyperphosphatemia as a result of urethral obstruction?
- re-establish GFR by decompressing the bladder or relieving obstruction
- IV fluid diuresis
What causes hypocalcemia as a result of urethral obstruction? What does this result in?
secondary to hyperphosphatemia - law of mass action
further compromises neuromuscular excitation (seizures!) and cardiac contractility
How is hypocalcemia as a result of urethral obstruction treated?
IV calcium gluconate
How can a tentative diagnosis of urethral obstruction be made? What diagnostics are recommended?
clinical presentation - straining to urinate, depression, distended/turgid bladder
- PCV/TP
- blood gas with electrolytes
- ECG
- blood glucose
- BUN
- BP
What are the 7 major steps to treating urethral obstructions?
- rehydration with potassium-free fluids (0.9% NaCl)
- address life-threatening electrolyte abnormalities with calcium, insulin, dextrose, and sodium bicarbonate
- relieve bladder obstruction with a urinary catheter to retropulse the obstruction back to the bladder, then place an indwelling catheter to prevent re-obstruction
- monitor urine production as post-obstructive diuresis is common (maintain IV fluids!)
- once patient is stabilized, identify and address underlying cause of obstruction, consider x-rays, abdominal U/S, UA, and urine culture
- analgesia and sedation
- leave catheter in place until azotemia, electrolyte abnormalities, and postobstructive diuresis is resolved –> observe 12-24 hours after catheter removal to ensure spontaneous urination
