Cerebral Salt Wasting

Also known as: CSW, Renal salt wasting

Cerebral salt wasting is a hyponatraemia occurring in the context of intracranial pathology, most classically subarachnoid haemorrhage, but also traumatic brain injury, neurosurgery, meningitis and intracranial tumours ,in which renal sodium loss produces genuine volume depletion alongside the low sodium.

Its clinical importance lies almost entirely in its distinction from SIADH, because the two look superficially similar on biochemistry but require opposite treatment: fluid restriction in SIADH, and salt and water replacement in cerebral salt wasting.

Restricting fluid in a patient who is actually volume deplete after subarachnoid haemorrhage worsens cerebral perfusion and risks precipitating delayed cerebral ischaemia.

Hyponatraemia in a patient with recent intracranial pathology, usually developing within the first week
Features of hyponatraemia itself: headache, nausea, confusion, lethargy, and seizures if severe or rapid
Signs of true volume depletion, which are the discriminating features: postural hypotension, tachycardia, dry mucous membranes, reduced skin turgor, low JVP, reduced urine output relative to intake, and a negative fluid balance on the chart
High urine output despite clinical hypovolaemia, which is the paradox at the centre of the syndrome

Biochemically, cerebral salt wasting and SIADH both show hyponatraemia with low plasma osmolality, concentrated urine and a high urine sodium. Volume status is the discriminator, and it is a clinical assessment rather than a laboratory one.

Careful, repeated assessment of volume status: fluid balance charts, daily weights, postural blood pressure, JVP, and response to a fluid challenge
Urine sodium is high in both conditions and does not distinguish them
Serum urea and uric acid tend to be higher in cerebral salt wasting (reflecting volume depletion) and lower in SIADH, though there is overlap and neither is definitive
Central venous pressure or non-invasive haemodynamic assessment may help in the intensive care setting
Exclude adrenal insufficiency and hypothyroidism as for any hyponatraemia

Differentials: SIADH (the principal one, and the distinction is the entire clinical question), adrenal insufficiency, and iatrogenic hyponatraemia from hypotonic intravenous fluids, which is common and easily overlooked in neurosurgical patients.

Volume and sodium replacement, which is the opposite of SIADH management: isotonic saline to restore euvolaemia, with hypertonic saline reserved for severe or symptomatic hyponatraemia
Fludrocortisone is used in some centres to reduce renal sodium loss, particularly after subarachnoid haemorrhage, with monitoring for hypokalaemia and fluid overload
Salt supplementation, oral or enteral, as an adjunct
The same correction-rate limits apply as for any hyponatraemia: no more than 8–10 mmol/L in 24 hours, given the risk of osmotic demyelination
Avoid fluid restriction — in the specific setting of subarachnoid haemorrhage this risks worsening cerebral perfusion and delayed cerebral ischaemia, which is why getting the diagnosis right rather than defaulting to SIADH management matters so much
Close neurological observation alongside biochemical monitoring

Referral: neurosurgery and intensive care, since these patients are almost always already under specialist care; endocrinology input may help where the distinction from SIADH remains genuinely unclear.

Clinical toolsCalculators

BMI GCS EDD Parkland Formula

Corrected Sodium Corrected Calcium Anion Gap Creatinine Clearance Insulin Calculations qSOFA Wells PE Wells DVT CHA₂DS₂-VASc HAS-BLED CURB-65 Centor/McIsaac

Urinary Tract Infection

Also known as: UTI

Bacterial infection of the urinary tract: lower UTI/cystitis (bladder) or upper UTI/pyelonephritis (kidney, more severe).

Predominantly E. coli (~80%), also Klebsiella, Proteus, Enterococcus, Staph saprophyticus (young sexually active women).

Classified: uncomplicated (healthy non-pregnant women, normal urinary tract) vs. complicated (male, pregnant, catheter, structural/functional abnormality, immunocompromised, recent instrumentation).

Cystitis: dysuria, frequency, urgency, suprapubic pain, hematuria: no fever/flank pain/systemic symptoms
Pyelonephritis: fever, rigors, flank/loin pain, costovertebral angle tenderness, nausea/vomiting, plus lower UTI symptoms often present; can progress to sepsis (see Sepsis entry)
Elderly: may present atypically: confusion, falls, functional decline, without classic urinary symptoms
Catheter-associated: often asymptomatic bacteriuria (do NOT treat unless symptomatic) vs. true infection (fever, new flank pain, altered mental status without other cause)

Uncomplicated cystitis in women with classic symptoms: clinical diagnosis sufficient, treat empirically without culture
Urine dipstick: nitrites (specific) and leukocyte esterase (sensitive) — supportive, not required if classic symptoms present
Urine culture: indicated for pyelonephritis, complicated UTI, treatment failure, recurrent UTI, pregnancy, men, catheterized patients — guides targeted therapy
Bloods (FBC, U&E, CRP, blood cultures): if systemically unwell/pyelonephritis/suspected sepsis
Imaging (renal ultrasound/CT): recurrent pyelonephritis, suspected obstruction/stone, failure to respond to treatment, males with first UTI (investigate underlying cause)
Asymptomatic bacteriuria: do not treat except in pregnancy or pre-urological instrumentation

Differentials: vaginitis/candidiasis (external dysuria, discharge), urethritis (STI-related), interstitial cystitis, pelvic inflammatory disease, appendicitis/renal colic (flank pain differentials), STI.

Uncomplicated cystitis (women):

Nitrofurantoin 100mg bd × 3-5 days (avoid if eGFR <45), or trimethoprim 200mg bd × 3 days (check local resistance), or fosfomycin 3g single dose
Increase fluid intake, urinary alkalinizers for symptom relief (limited evidence)

Pyelonephritis:

Outpatient (mild, tolerating oral, no red flags): oral ciprofloxacin 500mg bd × 7 days, or co-amoxiclav/cephalosporin per local resistance × 7-14 days
Inpatient (severe, vomiting, sepsis features, pregnancy): IV antibiotics (ceftriaxone, or ciprofloxacin), switch to oral once improving, total course 10-14 days
Identify/manage complications: renal/perinephric abscess (imaging if not improving in 48-72h), obstruction requiring drainage (stent/nephrostomy)

Recurrent UTI (≥2 in 6 months or ≥3 in 12 months): investigate underlying cause, post-coital prophylaxis if coitally-related, low-dose nightly prophylactic antibiotic (nitrofurantoin 50-100mg nocte) if conservative measures fail, vaginal estrogen in postmenopausal women (restores protective flora), consider methenamine hippurate as non-antibiotic option.

Men: always investigate for underlying cause (prostatic, structural) after first UTI — not considered "uncomplicated"; treat 7 days minimum, consider prostatitis if perineal pain/systemic symptoms (requires longer course, 2-4 weeks, quinolone/trimethoprim given prostate penetration).

Pregnancy: treat all bacteriuria (symptomatic and asymptomatic) — nitrofurantoin (avoid near term — neonatal hemolysis risk) or cephalexin; avoid trimethoprim in first trimester (folate antagonist) and avoid quinolones throughout.

Referral: urology for recurrent UTI in men, structural abnormality, stones, treatment-resistant disease; nephrology for recurrent pyelonephritis with renal impairment.

Cerebral Salt Wasting

Overview

Clinical Features

Diagnosis

Management

Overview

Clinical Features

Diagnosis

Management