Urinary Flashcards

Question

How is acute urinary retention managed

Answer 1

Immediate urethral catheterisation to resolve the retention. Ensure to measure the volume of drained post-catheterisation Underlying cuases should be treated accordingly: -enlarged prostate - appropraiate meds (typically tamsulosin) should be started -check CSU for infection - treat with abx if appropriate -review med chart for attribution TWOC (trial without catheter) attempted once underlying cause is treated and if voids successfully with a minimal residual volume then passes. If fails will be recatheterised. Further TWOCs can be attempted if fails but multiple failed TWOCs may warrant long term catheter, until definitive management arragned to treat underlying cause.

Answer 2

Few complications if caught and treated early In those with acute-on-chronic, AKI can occur which can lead to CHD if multiple episodes of retneiton leading to renal scarring other complcations of increased risk of UTIs and Renal stones due to urinary stasis

Answer 3

Men: -most common is BPH -other obstructive causes of urethral strictures or prostate cancer Women: -pelvic prolapse (such as cystocele, rectocele or uterine prolapse) -pelvic masses (such as large fibroids) Neurological causes: -peripheral neuropathies -upper motor neurone disease (Eg MS or Parkinson's)

Answer 4

Painless urinary retention Associated voiding LUTS wg weak stream and hesitancy with reduced functional capacity (the ability of the bladder to store urine before producing urge to void) Overflow incontinence whereby the intra-vesical pressures rise greated than those of the urinary sphincter. Usually worse at night (nocturnal enuresis) when the sphincter tone is reduced Palpable distended bladder with no or minimal tenderness Perform PR (in men) to assess for evidence of prostate enlargement

Answer 5

Refers to the urinary retention causing such high intra-vesicular pressures that the anti-reflux mechanism of the bladder and ureters is overcome and ‘backs up’ into the upper renal tract leading to hydroureter and hydronephrosis, impairing the kidneys’ clearance levels. Such patients present in retention with associated deranged renal function, and hydronephrosis will be subsequently confirmed on imaging (typically ultrasound as first line). Repeat episodes of high-pressure chronic retention can cause permanent renal scarring and chronic kidney disease (CKD). By contrast, low pressure retention occurs in patients with retention with the upper renal tract unaffected due competent urethral valves or reduced detrusor muscle contractility / complete detrusor failure.

Answer 6

Following resolution of the retention through catheterisation, the kidneys can often over-diurese due to the loss of their medullary concentration gradient, which can take time to re-equilibrate. This over-diuresis can lead to a worsening AKI. Consequently, those patients at risk should have their urine output monitored over the following 24 hours post-catheterisation. Patients producing >200ml/hr urine output should have around 50% of their urine output replaced with intravenous fluids to avoid any worsening AKI.

Answer 7

Due to stasis of urine, patients with chronic retention are more likely to develop urinary tract infections and form bladder calculi. Repeat episodes of unmanaged high-pressure retention can lead to chronic kidney disease.

Answer 8

Plasma potassium in excess of ≥ 5.5 mmol/L Further classified by the European resus guide as: Mild – 5.5-5.9 mmol/L Moderate – 6.0-6.4 mmol/L Severe – >6.5 mmol/L The incidence of complications rises with increasing severity of hyperkalaemia The rate at which serum potassium rises also is an important factor which influences the likelihood of complications occurring

Answer 9

Renal: In healthy individuals, the kidneys are responsible for 90% of potassium excretion, with the remainder excreted via the gastrointestinal tract. As a result, renal impairment is one of the commonest causes of hyperkalaemia. -Acute kidney injury (AKI) -Chronic kidney disease (CKD) -Hyperkalaemic renal tubular acidosis Iatrogenic: Many medications can cause or contribute to hyperkalemia directly or indirectly: -ACE inhibitors -Angiotensin receptor blockers -Potassium-sparing diuretics -NSAIDs/COX 2 inhibitors -Digoxin (in toxicity) -Trimethoprim -Beta-blockers – selective and non-selective can cause it -Nicorandil -Heparin – unfractionated and LMWH -Ciclosporin -Tacrolimus -Renin-inhibitors (e.g. aliskiren) -Potassium supplements Intravenous fluids containing potassium also have the potential to cause hyperkalaemia when prescribed inappropriately. Blood transfusion is another potential cause of hyperkalaemia. Trauma and burns: Tissue damage sustained secondary to trauma or burns results in the release of significant volumes of potassium from damaged cells. DKA: In diabetic ketoacidosis (DKA) potassium shifts from the intracellular to the extracellular space due to a lack of insulin, resulting in hyperkalaemia. Addison's: Aldosterone promotes excretion of potassium by the kidneys. In Addison’s disease, the adrenal glands are unable to produce adequate levels of aldosterone which results in reduced renal excretion of potassium.

Answer 10

Pseudohyperkalaemia can occur for a wide variety of reasons including: -Haemolysis (e.g. prolonged tourniquet time, prolonged sample transport time, use of incorrect blood bottles) -Blood sample being taken from a limb receiving IV fluids containing potassium -Leukocytosis and thrombocytosis If there are concerns about pseudohyperkalaemia, a sample should be urgently repeated to check the validity of the result.

Answer 11

Typically vague symptoms of general weakness and fatigue May sometimes experience: -palpitations -chest pain -SOB No obvious signs of hyperkalaemia usually Potentially: -bradicardia secondary to hyperkalaemia0induced atrioventricular block -depressed or absent tendon reflexes

Answer 12

U&Es should be performed to: -confirm the presence of hyperkalaemia and assess other electrolytes (a repeat sample should be sent if hyperkalaemia is noted) -assess renal function (the kidneys are responsible for 90% of potassium excretion) FBC should be performed to: -rule out haemolysis (e.g. normocytic normochromic anaemia) -rule out leukocytosis or thrombocytosis Capillary blood glucose should be performed to rule out hyperglycaemia (e.g. DKA). An arterial blood gas should be performed to rule out metabolic acidosis (e.g. hyperkalaemic renal tubular acidosis or DKA). Serum cortisol should be performed to rule out Addison’s disease (low serum cortisol is found in Addison’s). A digoxin level should be performed to rule out toxicity (if relevant). An ECG is an essential investigation in the context of hyperkalaemia, abnormalities can include: -Tall tented T waves -Wide QRS complexes -Prolonged PR interval -Flattened P waves -AV block -Bradycardia

Answer 13

The urgency by which hyperkalemia needs to be treated is determined by the level of potassium and the presence/absence of associated ECG changes. A potassium level of ≥7.0 mmol/L and/or a patient with hyperkalaemia associated ECG changes requires URGENT treatment. All patients with hyperkalaemia will ultimately require some form of further monitoring and management. Step 1.Prevent further accumulation of potassium: -Stop any intravenous fluids containing potassium -Suspend any medications that have the potential to increase serum potassium -Suspend any supplements containing potassium Step 2.Stabilise the cardiac membrane: -Administer intravenous calcium gluconate (10mls of 10% solution) if there are hyperkalaemia associated ECG changes present. This should help to stabilise the myocardium temporarily for 30-60 minutes and reduce the risk of fatal arrhythmia. -Further doses may be required if ECG changes persist (you would expect ECG changes to begin to improve within 1-3 minutes from the administration of calcium gluconate). The administration of calcium gluconate in the absence of hyperkalaemia associated ECG changes is not recommended. Step 3.Shift potassium intracellularly: -Insulin-glucose infusion: insulin helps to shift potassium from the extracellular to the intracellular compartment, whilst the glucose helps to maintain capillary blood glucose levels. -Salbutamol: often used as adjuvant therapy for hyperkalaemia as it promotes the movement of potassium into cells and therefore out of the serum. Step 4.Remove potassium from the body: -Calcium polystyrene sulfonate resin (Calcium resonium) can be used to remove potassium via the gastrointestinal tract. -Correction of the underlying cause: the kidneys should then be able to resume their normal function of excreting adequate volumes of potassium via the urine. -Haemodialysis is an invasive treatment reserved as a last resort for resistant hyperkalaemia that has failed to respond to all other therapies.

Urinary Flashcards

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