Decreased Urine Output

Phone Call/Presentation Questions

• What is the urine output? (How much urine has been passed in the past 24 hours)
  • Oliguria = urine output <400mL/day (<20mL/h)
  • Anuria ⇒ mechanical obstruction of bladder outlet, blocked IDC or obstructed single kidney
  • How are we measuring this and why?
  • How much does the patient weigh?
• Does the patient have abdominal pain?
  • Generalised abdominal pain ⇒ ? acutely distended bladder with urinary retention
• Is the patient eating and drinking?
• Other observations?
• Does the patient have an indwelling urinary catheter?
• Reason for admission?
• Does the patient have an IVC?

Instructions

• If IDC in place and the patient is anuric ask the nurse to flush the catheter with 20-30mL of normal saline
• Request blood for FBC, UEC and creatinine
  • Serum potassium of >5.5mmol/L ⇒ Hyperkalaemia

Prioritisation

• Urgently assess patient with painful urinary retention with urine output <20mL/h or daily urine output of <400mL
  • Can be a sign of AKI which can cause hyperkalaemia and fluid overload
• Otherwise can wait for high-priority problems, provided patient is not in pain and serum potassium is not elevated

Common Causes (Corridor thoughts)

• Normal urine output in a healthy individual should be between 0.5-1.5 mL/kg/hour, and patients should generally be urinating at least every 6 hours (Geeky Medics: Measuring & Recording Urine Output).
• Pre-renal
  • Absolute decrease in circulating blood volume causing hypoperfusion:
    • Inadequate fluid intake e.g. after surgery
    • Increased loss of blood or fluids (haemorrhage, burns, erythroderma, hypertheymia, GI fluid losses such as vomiting, diarrhoea, NG suction, renal losses such as diuretics and glycosuria)
    • Third spacing of fluid e.g. in pancreatitis, bowel obstruction
  • Cardiac failure
    • MI (cardiogenic shock), CCF
  • Effective decrease in blood volume (vasodilation)
    • Sepsis, anaphylaxis, neurogenic Shock
    • Vasodilatory drugs, anaesthetic drugs
  • Obstruction to circulation
    • Constrictive pericarditis, cardiac tamponade, PE
  • Locally reduced renal perfusion
    • Renal artery or renal vein occlusion (2° thrombosis or stenosis)
    • Noradrenaline, adrenaline
    • NSAIDs, ACE-i
• Intra-renal
  • Acute tubular necrosis
    • Usually 2° to pre-renal causes
    • Medications (e.g. aminoglycosides, amphotericin B, IV contrast, chemotherapy)
    • Poisons (e.g. ethylene glycol, mercury, carbon tetrachloride)
    • Endogenous substances (e.g. myoglobin, Bence-Jones protein, amyloid)
  • Glomerulonephritis
  • Interstitial nephritis
    • Pyelonephritis
    • Medications (e.g. NSAIDs, penicillins, cephalosporins, sulfonamides, ciprofloxacin, rifampicin)
    • Malignancy (e.g. lymphoma or leukaemia)
    • Systemic disorder (SLE, sarcoidosis, hypercalcaemia)
• Post-renal
  • Upper renal tract obstruction
    • Stone, blood clot, sloughed papilla (single kidney)
    • Retroperitoneal fibrosis, retroperitoneal tumour
  • Lower urinary tract obstruction (bladder outlet obstruction)
    • Prostatic hypertrophy, carcinoma of the cervix
    • Stone, blood clot, urethral stricture
  • Catheter blockage

WARNING

• A reduced urine output may be the earliest manifestation of shock; restoration of urine output >0.5mL/kg/h signifies restoration of adequate renal perfusion
• Oliguric acute renal failure may be associated with hyperkalaemia, hypertension or acute pulmonary oedema
• Sequelae of acute renal failure include:
  • Hyperkalaemia
  • Metabolic acidosis
  • Acute hypertension (see Hypertension)
  • Pulmonary oedema secondary to salt and water retention

Assessment

End of Bed

• How does the patient look?
  • A restless patient with abdominal discomfort, agitation and a sensation of needing to pass urine suggests an acutely distended bladder
  • Sometimes urinary retention and/or ↓ urine output can have no obvious problems

A → E Assessment

• Heart rate and blood pressure?
  • ↑HR by >20 beats/min + ↓SBP by >20mmHg or any ↓DBP ⇒ significant hypovolaemia → pre-renal hypoperfusion
  • However ↑HR alone may be due to ↓ intravascular volume, pain of distended bladder or infection
  • Acute hypertenstion with oedema may result from acute glomerulonephritis
• Temperature?
  • Fever suggests sepsis which could be 2° to UTI, pyelonephritis or systemic bacteraemia

Selective History and Chart Review

• Review patient’s history and hospital course looking for factors that predispose to pre-renal, renal or post-renal causes of decreased urine ouptput with ANKI
• Review observations and fluid balance chart for fluctuations in fluid intake, urine output and body weight
• Medication chart:
  • Nephrotoxic drugs, especially in combination such as ACE-i with diuretic and NSAID; aminoglycoside with amphoterecin B; IV contrast material with an ACE-i; or a patient in CCF given an NSAID
  • Dose the onset coincide with the commencement of the nephrotoxic drug?
  • Potassium supplements worsen hyperkalaemia
• Recent blood urea and creatinine values
  • Urea-to-creatinine ratio >20 with specific gravity of >1.020 or urine sodium concentration of <20mmol/L suggests a pre-renal cause
  • Urea-to-creatinine ratio <10 with urine specific gravity of <1.020 or urine sodium concentration of >20mmol/L suggests a intrinsic renal cause (e.g. ATN)

Examination

Examination	Notes
Vital signs	Repeat now
	Note skin temperature and colour
	Tachycardia or postural BP changes from dehydration
	Hypertension
Mental status	Altered mental status ⇒ cerebral hypoperfusion, uraemic encephalopathy
HEENT	Jaundice (hepatorenal syndrome)
	Scleroderma facies
	Dry tongue and mucous membranes ⇒ dehydration
Resp	Basal crepitations, pleural effusions ⇒ CCF
	Tachypnoea ⇒ CCF or hypoventilation in metabolic acidosis
	Pleuritic chest pain ⇒ uraemia, SLE, neoplasm
CVS	Pulse volume
	↑ JVP ⇒ CCF
	↓ JVP/flat neck veins ⇒ dehydration
	Pericardial friction rub ⇒ uraemia, SLE, neoplasm
GIT	Enlarged kidneys ⇒ hydronephrosis 2° to obstruction, polycystic kidney disease
	Enlarged bladder ⇒ bladder outlet obstruction, blocked IDC, neurogenic bladder
Rectal	Enlarged prostate gland ⇒ bladder outlet obstruction
Pelvic	Cervical or adnexal masses ⇒ ureteric obstruction 2° to cervical, uterine or ovarian cancer
Skin	Rash ⇒ acute interstitial nephritis
	Livedo reticularis on lower extremities ⇒ hypoperfusion, embolic renal failure 1
	Pruritic excoriation ⇒ uraemia, drug rash

Investigations

• Take bloods for FBC, UEC and blood glucose
  • UEC: look for hyperkalaemia
  • FBC: Normal Hb suggests acute renal impairment whereas ↓ Hb suggests chronic renal impairment
• LFTs, autoantibodies accordingly as suspected
• VBG for raised anion gap metabolic acidosis from uraemia
• Glomeruloneohritis concern
  • Complements C3, C4
    • Lupus ANA dsDNA
    • Endocarditis multiple blood cultures
    • Cryoglobulonaemia usually occurs because of hep C
    • PT3 ANCA for ANCA positive vasculitis
• Perform ECG
  • Look for signs of hyperkalaemia: peaked T waves, depressed ST segments, prolonged PR interval, loos of P waves and wide QRS complexes
  • Look for evidence of MI or the widespread concave elevation of pericarditis
• Urine dipstick
  • If normal CT and no concern for UTI consider a glomerulonephritis to be the underlying cause
• Bedside bladder scan to measure residual bladder volume in obstruction
• Collect urine for dipstick analysis and send to laboratory for MCS including cells and casts, plus urinary electrolyte testing
  • Specific gravity
    • SG >1.025: highly concentrated urine associated with dehydration and pre-renal failure
    • SG 1.010: may be associated with chronic renal disease
    • SG <1.005: inability to concentrate urine (ATN, pyelonephritis)
  • Haematuria (stone disease, pyelonephritis, GN with >70% dysmorphic RBC)
  • Proteinuria (nephrotic syndrome, GN, pyelonephritis, CCF, myeloma)
  • Leucocytes and nitrites (UTI, pyelonephritis)
  • Urine microscopy
    • Leucocytes, Gram-stained organisms, erythrocytes, epithelial cells
    • RBC casts are diagnostic of GN
    • WBC casts (especially eosinophil casts) are seen in acute interstitial nephritis
    • Pigmented granular casts are seen with ATN
    • Oval fat bodies are suggestive of nephrotic syndrome

Immediate Management

NOTE

Every evaluation for ↓ urine output should begin with ruling out urinary retention

• Nil IDC present:
  • Check post void residual volume with a bladder scan and assess for urinary retention
  • Insert an IDC to accurately monitor fluid balance
    • Lower urinary tract obstruction by insertion of an IDC
      • If there has been bladder outlet obstruction, the initial urine volume on catheterisation is usually >400 mL and the patient experiences immediate relief
      • After catheterisation for urinary retention, watch for a post-obstructive diuresis by measuring urine volumes hourly
• IDC present:
  • Ensure IDC is not clogged or kinked
    • Flush a blocked IDC with 20-30mL sterile normal saline to resolve intraluminal blockage causing anuria
• If obsstruction is ruled out:
  • Assess volume status based on history, clinical situation, JVP and IVC ultrasound (do not give IV fluids to a patient in urinary retention)
• Assess for kidney injury using bloods and urinalysis
• Rule out emerging sepsis
• Attach continuous non-invasive ECG, BP and pulse oximeter monitoring to the patient

Life Threatening Complications

• Severe hyperkalaemia:
  • Give 10% calcium chloride 10mL IV over 2-3 minutes to provide immediate cardioprotection to prevent cardiac arrest
  • Reduce serum potassium level:
    • Give 50mL of 50% dextrose IV with 10 units of soluble insulin over 20 minutes
    • Give salbutamol 5-10mg nebulised or 200-500mcg salbutamol IV slowly; repeat doses may be given
    • Give 8.4% sodium bicarbonate ($\mathrm{NaHCO}{}_3{}^{-}$) 50mL IV over 5 minutes if the patient is acidotic, provided there is no volume overload; works best in combination with dextrose/insulin therapy and salbutamol
    • Follow up with potassium exchange resin: calcium resonium 30g PO or enema
• Hypotension with intravascular depletion
  • Restore the intravascular volume with normal saline in pre-renal failure; give IV fluid bolus 20mL/kg normal saline repeatedly as needed
  • Observe the effect of this fluid challenge on the pulse, JVP, BP and urine output aiming to optimise renal perfusion by reversing hypovolaemia
• Acute pulmonary oedema
  • See APO
  • In addition to upright, oxygen, gtn, frusemide:
    • Give frusemide if pre-renal perfusion is normal
    • Consider CPAP and/or IV GTN after consultation with senior doctor
    • Monitor diuresis with hourly urine measures and frequent checks of vital signs
    • Arrange urgent dialysis if the patient remains volume overloaded, severely acidotic and/or hyperkalaemic

Specific Management

• Identify cause and cease all inappropriate medications (Potassium supplements and potassium-sparing diuretics, NSAIDs, ACE inhibitors)
  • Leave a note to inform the usual medical team if on call
• Reduce the dose of renally excreted medications that cannot be stopped immediately (e.g. aminoglycosides)
• Consider indications for dialysis; consult senior and call ICU:
  • Hyperkalaemia (>6.5mmol/L) refractory to conventional therapy
  • Severe and symptomatic metabolic acidosis (pH <7.1)
  • Fluid overload unresponsive to diuretics
  • Uraemic encephalopathy with symptoms of decreased mental status, obtundation and seizures or uraemic pericarditis

Other Considerations

• Consider getting the nursing staff to do a two hourly bladder scan

Footnotes

Footnotes

1. Source: https://dermnetnz.org/topics/livedo-reticularis ↩