Learn — Renal, urinary & fluid–electrolytes

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Renal stone and renal cancer

Urolithiasis is the formation of stones anywhere in the urinary tract when urine becomes supersaturated and crystals nucleate and grow, while renal cell carcinoma is the commonest malignant tumour of the kidney and arises from proximal tubular epithelium. They are taught together because both present with loin pain and haematuria, and the discrimination matters — one is an emergency of obstruction and infection, the other a disease of staging and surgery in which painless haematuria must never be dismissed.

Stone types: calcium oxalate accounts for about 70 to 80% and is radio-opaque, arising from a low urine volume, hypercalciuria and hyperoxaluria; calcium phosphate forms in alkaline urine and in renal tubular acidosis; struvite or triple phosphate (magnesium ammonium phosphate) forms only in urine infected with urease-producing organisms such as Proteus, Klebsiella and Pseudomonas, and is the stone that grows into a staghorn calculus; uric acid stones are radiolucent, form in persistently acid urine in gout, high purine intake and after chemotherapy, and are the only common stone that can be dissolved by alkalinising the urine to pH 6.5 to 7; cystine stones are rare, faintly opaque and hereditary.
Ureteric colic is sudden, severe, colicky pain from the loin to the groin with the patient unable to keep still — the opposite of the motionless patient with peritonitis — accompanied by nausea, vomiting and microscopic haematuria, and referred to the testis or labium as the stone reaches the lower ureter. The three sites of impaction are the pelvi-ureteric junction, the crossing of the iliac vessels at the pelvic brim, and the vesico-ureteric junction, which is the narrowest point of all.
Non-contrast CT of the kidneys, ureters and bladder is the gold standard investigation, over 95% sensitive and able to show radiolucent stones; ultrasound is used first in pregnancy and in children, and a plain film shows only the radio-opaque stones and is useful for follow-up. Send urine for microscopy and culture and check creatinine, calcium and uric acid.
Treatment of colic: a non-steroidal anti-inflammatory such as diclofenac 75 mg intramuscularly relieves renal colic better than an opioid because it reduces the ureteric and intrarenal pressure; give an antiemetic and enough fluid to maintain output but do not force-load fluids into an obstructed system. About 80% of stones under 5 mm pass spontaneously, and medical expulsive therapy with tamsulosin 0.4 mg daily helps a lower ureteric stone of 5 to 10 mm. Strain all urine so a passed stone can be analysed.
Intervention: extracorporeal shock wave lithotripsy for smaller renal and upper ureteric stones, ureteroscopy with laser fragmentation for ureteric stones, and percutaneous nephrolithotomy for a stone over 2 cm or a staghorn calculus. Prevention is a fluid intake sufficient to produce 2.5 litres of urine a day, reduced salt and animal protein, a normal rather than a low dietary calcium, and potassium citrate or thiazide depending on the stone type.
Renal cell carcinoma is clear cell in about 75 to 80% of cases; risk factors are smoking, obesity, hypertension, acquired cystic disease in dialysis patients and von Hippel-Lindau disease. The classical triad of haematuria, loin pain and a loin mass occurs in under 10% and means advanced disease, and more than half are now found incidentally on imaging done for something else.
Renal cell carcinoma is called the internist's tumour for its paraneoplastic effects: polycythaemia from erythropoietin, hypercalcaemia from parathyroid hormone-related peptide, hypertension from renin, Stauffer's syndrome of non-metastatic hepatic dysfunction, and pyrexia of unknown origin. A left-sided varicocele that does not empty on lying down suggests obstruction of the left renal vein, and the tumour characteristically grows along the renal vein into the inferior vena cava and metastasises to the lung as cannonball secondaries, and to bone, liver and brain.
Staging is by contrast CT of abdomen and chest. Partial or nephron-sparing nephrectomy is used for T1 tumours up to 7 cm and radical nephrectomy for larger ones; the tumour is resistant to conventional radiotherapy and chemotherapy, so advanced disease is treated with tyrosine kinase inhibitors and immune checkpoint inhibitors. In children the equivalent tumour is Wilms tumour (nephroblastoma), presenting at 3 to 4 years with a smooth abdominal mass that does not cross the midline and which should not be palpated repeatedly.

Horseshoe kidney

Horseshoe kidney is the commonest fusion anomaly of the urinary tract, in which the lower poles of the two kidneys are joined across the midline by an isthmus of renal parenchyma or of fibrous tissue. It matters far beyond its rarity value in an exam: the fused kidney sits low, unrotated and unprotected in front of the vertebral column, so it obstructs, infects and forms stones, is more exposed to blunt abdominal trauma, and can be injured during aortic, retroperitoneal or colorectal surgery by a surgeon who did not know it was there.

It occurs in roughly 1 in 400 to 500 people and is about twice as common in males; the isthmus is functioning renal parenchyma in the majority and fibrous tissue in the remainder.
Embryologically the two metanephric masses fuse at their lower poles in the fourth to sixth week; as the kidneys ascend, the isthmus is caught beneath the inferior mesenteric artery at about the level of the third or fourth lumbar vertebra, so ascent stops early and rotation is never completed — the renal pelves face forwards and the ureters pass anteriorly over the isthmus.
The blood supply is variable and multiple, with aberrant vessels arising from the aorta, the common and external iliac arteries and the inferior mesenteric artery; this is the single most important operative fact about the anomaly and the reason it must be flagged before any abdominal or aortic operation.
The anteriorly running ureter and the high insertion of the renal pelvis cause pelvi-ureteric junction obstruction and urinary stasis, which is why the classic complications are hydronephrosis in about a third of patients, recurrent urinary infection and stone formation; vesico-ureteric reflux is also more common.
Most horseshoe kidneys are silent and are found incidentally on imaging done for another reason; when symptomatic there is vague central or lower abdominal pain, a palpable midline mass, or Rovsing's sign for this condition — abdominal pain with nausea and vomiting brought on by hyperextension of the spine, which stretches the isthmus over the vertebral bodies.
Associations to remember: horseshoe kidney is strongly associated with Turner syndrome (45,XO) and with trisomy 18, and it carries an increased risk of Wilms tumour in children, of transitional cell carcinoma of the renal pelvis, and characteristically of renal carcinoid tumour.
Diagnosis is by ultrasound and confirmed with contrast CT or CT urography, which also maps the aberrant vessels; a diuretic renogram with MAG3 or DTPA measures split function and confirms whether a dilated system is truly obstructed.
Management is to treat only what the anomaly causes: nothing at all for the asymptomatic kidney, pyeloplasty for pelvi-ureteric junction obstruction, percutaneous nephrolithotomy in preference to shock wave lithotripsy for stones because fragments drain poorly from a low, malrotated pelvis, and antibiotics with source control for infection. Division of the isthmus is now rarely performed.
Nursing points: teach a high fluid intake and early reporting of urinary symptoms because stasis makes infection likely, ensure the anomaly is recorded prominently before any abdominal surgery or trauma imaging, and remember that the kidney lying across the vertebral bodies without the protection of the lower ribs is more easily crushed in a direct blow to the abdomen.

Bladder cancer

Bladder cancer is malignancy of the urothelial lining of the bladder, of which more than 90% is urothelial (transitional cell) carcinoma. It matters because painless visible haematuria is usually its only symptom, and because the whole urothelium shares the same carcinogen exposure — a field change that makes recurrence the rule and lifelong surveillance necessary.

Cigarette smoking is the single largest risk factor, accounting for around half of all cases and raising risk three to four fold; occupational exposure to aromatic amines such as beta-naphthylamine and benzidine in the dye, rubber, leather, paint and printing industries is the classic second; cyclophosphamide through its metabolite acrolein, pelvic radiotherapy, and chronic irritation from a long-term catheter or stones also contribute.
Histology follows the cause: transitional cell carcinoma is the default, squamous cell carcinoma follows chronic irritation and Schistosoma haematobium infection (endemic in Egypt and the Middle East), and adenocarcinoma arises in a urachal remnant or in bladder exstrophy.
Presentation is painless, intermittent, visible haematuria in about 80 to 90%; irritative symptoms of frequency, urgency and dysuria with sterile pyuria and no infection on culture suggest carcinoma in situ, which is flat and non-invasive yet high grade and dangerous.
Investigation: cystoscopy with biopsy is the gold standard and every adult with painless visible haematuria needs it; CT urography images the upper tracts because the same field change causes ureteric and renal pelvic tumours, and urine cytology is most useful for high-grade disease and carcinoma in situ.
Staging drives the treatment. Non-muscle-invasive disease — Ta papillary, T1 into the lamina propria, and carcinoma in situ — is treated by transurethral resection of the bladder tumour with a single immediate post-operative intravesical dose of chemotherapy such as mitomycin C, with a course of intravesical BCG for high-risk tumours and carcinoma in situ. Muscle-invasive disease from T2 upwards needs radical cystectomy with urinary diversion by ileal conduit or neobladder, usually with neoadjuvant cisplatin-based chemotherapy, or bladder-preserving chemoradiation.
Recurrence occurs in up to 70% of non-muscle-invasive tumours, so surveillance cystoscopy is done at 3 months and then at lengthening intervals for life; smoking cessation is part of the treatment, not merely advice.
Nursing after transurethral resection: a three-way catheter runs continuous bladder irrigation, and the nurse watches the colour of the effluent, keeps the output balanced against the irrigation input, and acts on clot retention. After intravesical BCG the patient holds the instillation for 2 hours turning position every 15 minutes, must not receive it after a traumatic catheterisation or with an active infection or haematuria, and should sit to void and disinfect the toilet with bleach for 6 hours afterwards. After an ileal conduit, teach stoma care and explain that mucus in the urine is normal.

Nephrotic syndrome

Nephrotic syndrome is the clinical picture produced by a glomerular filtration barrier that has become leaky to protein: heavy proteinuria of more than 3.5 g per 1.73 square metres per day in an adult, hypoalbuminaemia, generalised oedema and hyperlipidaemia with lipiduria. It matters at the bedside because the same protein loss that causes the swelling also strips away immunoglobulin and antithrombin, so these patients are killed by infection and thrombosis rather than by the swelling itself.

The diagnostic quartet is proteinuria above 3.5 g a day in adults (in children a urine protein-to-creatinine ratio above 2 mg/mg, or 3+ to 4+ dipstick protein on three consecutive days), a serum albumin below about 2.5 g/dL, oedema and hyperlipidaemia; frothy urine and periorbital puffiness that is worst on waking are the classic complaints.
The oedema is soft and pitting, begins around the eyes and moves with gravity through the day to the legs, and in severe cases becomes ascites, pleural effusion and anasarca with rapid weight gain.
In children under 10 about 90% of cases are minimal change disease, which is steroid responsive and comes with a normal blood pressure, no haematuria and normal renal function, so a biopsy is not done first; biopsy is reserved for steroid resistance, age under 1 year or over 12 years, hypertension, persistent haematuria, low complement or impaired renal function.
In adults the common causes are focal segmental glomerulosclerosis, membranous nephropathy (look for the anti-PLA2R antibody) and diabetic nephropathy, with amyloidosis, lupus, hepatitis B and C and drugs behind them, and adults are biopsied.
The discriminator against NEPHRITIC syndrome is the urinary sediment: nephrotic urine is bland with heavy protein and oval fat bodies, while nephritic urine contains red cells and RED CELL CASTS with hypertension, oliguria and only modest proteinuria.
The complications that kill are infection — spontaneous bacterial peritonitis and cellulitis, usually pneumococcal, because IgG and complement factor B are lost in the urine — and venous thrombosis, especially renal vein thrombosis in membranous nephropathy, because antithrombin III is lost; hypovolaemia, acute kidney injury and accelerated atherosclerosis follow behind.
Treatment of childhood minimal change disease is prednisolone 60 mg per square metre a day up to a maximum of 60 mg for 4 to 6 weeks, then 40 mg per square metre on alternate days for a further 4 to 6 weeks, with steroid-sparing agents such as levamisole, cyclophosphamide, calcineurin inhibitors or rituximab for frequent relapses and steroid dependence.
Supportive management is salt restriction, cautious loop diuretics only when the patient is not hypovolaemic, an ACE inhibitor or ARB to reduce proteinuria in adults, statins for the lipids, adequate protein and calorie intake without severe protein restriction, and pneumococcal vaccination with live vaccines deferred while on high-dose steroids.
The nursing observations that make this manageable are a daily weight on the same scale at the same time in the same clothes, strict intake and output, abdominal girth, blood pressure and a daily urine dipstick for protein — the weight is the single most reliable measure of the oedema.

Chronic renal failure

Chronic kidney disease is an abnormality of kidney structure or function present for more than three months — either a glomerular filtration rate below 60 mL/min/1.73 m2 or a marker of damage such as albuminuria, an abnormal sediment, a structural abnormality or a transplanted kidney. It is irreversible and progressive, so the work is to slow the decline, treat the complications the failing kidney produces, and prepare the patient for dialysis or transplantation before they arrive as an emergency.

Staging uses the GFR and the albuminuria together: G1 is a GFR of 90 or more with evidence of damage, G2 is 60 to 89, G3a is 45 to 59, G3b is 30 to 44, G4 is 15 to 29 and G5 is under 15 mL/min/1.73 m2; albuminuria is A1 under 30, A2 30 to 300 and A3 above 300 mg of albumin per gram of creatinine.
The two commonest causes in India are diabetes and hypertension, followed by chronic glomerulonephritis, obstructive uropathy and chronic interstitial disease including analgesic and unregulated traditional-medicine nephropathy.
Anaemia comes from failure of erythropoietin production and is normocytic and normochromic; iron stores are repleted first and an erythropoiesis-stimulating agent is started when the haemoglobin falls below about 10 g/dL, aiming at partial correction rather than a normal haemoglobin.
Mineral and bone disorder runs as a chain: phosphate retention and low calcitriol lower the calcium, which drives secondary hyperparathyroidism and renal osteodystrophy, managed with dietary phosphate restriction, phosphate binders taken WITH food, active vitamin D and calcimimetics.
The metabolic complications to expect are hyperkalaemia, a high anion gap metabolic acidosis treated with oral sodium bicarbonate to keep the serum bicarbonate at 22 mEq/L or above, fluid overload with hypertension and pulmonary oedema, hyperuricaemia, and finally uraemia with nausea, hiccups, pruritus, a metallic taste, encephalopathy and pericarditis.
Slowing progression rests on blood pressure control with an ACE inhibitor or ARB titrated to the maximum tolerated dose in albuminuric disease, an SGLT2 inhibitor for chronic kidney disease with albuminuria, tight glycaemic control, salt restriction below 5 g of salt a day, stopping smoking, avoiding NSAIDs, aminoglycosides and unnecessary contrast, and a protein intake around 0.8 g/kg a day rather than severe restriction.
Serum creatinine and potassium are rechecked 1 to 2 weeks after starting or increasing an ACE inhibitor or ARB: a creatinine rise of up to about 30% is expected and acceptable, while a larger rise or hyperkalaemia means stopping the drug and looking for renal artery stenosis or volume depletion.
Preparation for kidney replacement therapy starts early with education about haemodialysis, peritoneal dialysis and transplantation, creation of an arteriovenous fistula months before it is needed, hepatitis B vaccination, and preservation of the forearm veins by using the back of the hand for cannulation.
Dialysis is started for uraemic symptoms, refractory fluid overload, hyperkalaemia or acidosis that will not correct, or pericarditis, usually as the GFR falls below about 10 mL/min/1.73 m2, while transplantation gives the best survival and quality of life.

Nephrectomy

Nephrectomy is the surgical removal of a kidney: radical nephrectomy takes the kidney with the perirenal fat and Gerota fascia and sometimes the adrenal gland and regional nodes for cancer, partial or nephron-sparing nephrectomy removes only the tumour and spares the rest, simple nephrectomy removes a chronically infected or non-functioning kidney, and donor nephrectomy takes a healthy kidney for transplantation. The nursing weight of the operation lies in the two things that go wrong fastest afterwards — bleeding from a highly vascular retroperitoneal bed, and a urine output that must now come from one kidney alone.

Indications are renal cell carcinoma (the commonest), Wilms tumour in children, a non-functioning kidney from chronic obstruction or infection, xanthogranulomatous or tuberculous pyonephrosis, irreparable trauma, refractory renovascular hypertension and live kidney donation.
Renal cell carcinoma classically presents with the triad of flank pain, a palpable mass and haematuria, but the full triad appears in fewer than 10% of patients and most tumours today are found incidentally on ultrasound or CT done for something else.
The function of the OTHER kidney must be documented before surgery with creatinine, eGFR and imaging, and a radionuclide renogram when there is doubt, because after a radical nephrectomy the remaining kidney is all the patient has.
The flank or loin incision cuts across the muscles just below the diaphragm, so post-operative pain limits breathing: the highest early risk is atelectasis and pneumonia, and the answer is adequate analgesia first, then splinting the incision with a pillow for coughing, deep breathing exercises, incentive spirometry every hour while awake and early mobilisation.
If the eleventh or twelfth rib was resected the pleura may have been breached, so watch for sudden breathlessness, chest pain, reduced air entry and tracheal shift, because pneumothorax is a recognised complication of the loin approach.
Urine output is the critical observation: report an output below 30 mL/h in an adult, or under 0.5 mL/kg/h, sustained over two hours, because it may mean hypovolaemia, ureteric injury or failure of the remaining kidney; measure it hourly for the first 24 to 48 hours, keep the catheter draining freely and record each drain separately.
Haemorrhage into the retroperitoneum can be hidden — look for a rising pulse, a falling blood pressure, restlessness, flank or back pain, abdominal distension, a bulging flank, blood on the dressing and a falling haemoglobin, because a retroperitoneal bleed may never appear in the drain.
Paralytic ileus is common after handling the retroperitoneum, so keep the patient nil by mouth until bowel sounds and flatus return, decompress with the nasogastric tube if one is in place and mobilise early.
Discharge teaching for a patient with one kidney is to drink enough to keep the urine pale, to avoid NSAIDs, other nephrotoxic drugs and unsupervised herbal or traditional preparations, to treat urinary infections promptly, to avoid contact sports that risk a blow to the flank, and to have blood pressure, serum creatinine and urine protein checked at least once a year for life.

Acute kidney injury

Acute kidney injury is an abrupt fall in glomerular filtration over hours to days, recognised by a rise in serum creatinine or a fall in urine output, and it is often reversible if the cause is found and removed early. It matters because it happens on every ward — to the hypotensive post-operative patient, the septic patient, the dehydrated child, the patient given contrast or an NSAID — and because the nurse's fluid balance chart is usually the first place it shows.

The KDIGO definition is any one of a rise in serum creatinine of 0.3 mg/dL or more within 48 hours, a rise to 1.5 times the baseline known or presumed to have occurred within 7 days, or a urine output under 0.5 mL/kg/h for 6 hours.
Staging: stage 1 is creatinine 1.5 to 1.9 times baseline or a rise of 0.3 mg/dL, or urine output under 0.5 mL/kg/h for 6 to 12 hours; stage 2 is 2.0 to 2.9 times baseline, or urine output under 0.5 mL/kg/h for 12 hours or more; stage 3 is 3 times baseline or a creatinine of 4.0 mg/dL or more, or the start of renal replacement therapy, or urine output under 0.3 mL/kg/h for 24 hours or anuria for 12 hours.
Causes are classified by site. Pre-renal, the commonest, is reduced perfusion from hypovolaemia, haemorrhage, sepsis, heart failure or drugs such as NSAIDs and ACE inhibitors. Intrinsic is damage to the kidney itself, chiefly acute tubular necrosis from prolonged ischaemia or toxins, acute interstitial nephritis from drugs, and glomerulonephritis. Post-renal is obstruction from stones, an enlarged prostate, a blocked catheter or pelvic malignancy.
Pre-renal injury and acute tubular necrosis are separated by the urine: pre-renal has a urine sodium under 20 mEq/L, a fractional excretion of sodium under 1%, a high urine osmolality above 500 mOsm/kg, a urea-to-creatinine ratio above 20 to 1 and a bland sediment, while acute tubular necrosis has a urine sodium above 40 mEq/L, a fractional excretion above 2%, an isosthenuric urine around 300 mOsm/kg and muddy brown granular casts.
The first three bedside actions when the urine output falls are to check that the catheter is patent and not kinked, to assess volume status and give a fluid challenge if the patient is dry, and to review and stop every nephrotoxic drug — NSAIDs, aminoglycosides, vancomycin, ACE inhibitors and ARBs in a hypovolaemic patient, and contrast.
Bladder scanning or catheterisation separates obstruction from failure within minutes and must not be forgotten, because relieving a blocked outlet reverses the injury at once; ultrasound of the kidneys, ureters and bladder is the standard first imaging.
The indications for urgent dialysis are remembered as AEIOU: refractory Acidosis, Electrolyte disturbance and especially a potassium above 6.5 mEq/L or with ECG changes, Ingestion of a dialysable poison, fluid Overload unresponsive to diuretics, and Uraemic complications such as pericarditis, encephalopathy or bleeding.
Rhabdomyolysis causes acute kidney injury after crush injury, prolonged immobility, seizures or extreme exertion: the creatine kinase is very high, the urine is tea-coloured, and the dipstick reads positive for blood while microscopy shows no red cells; treatment is early and generous intravenous fluid to keep the urine flowing.
Nursing management is measurement — hourly urine output, daily weight, strict intake and output, blood pressure and heart rate, daily creatinine, urea and electrolytes, a potassium-restricted diet and drug doses adjusted to the falling GFR — plus a clear note in the record that this patient has had acute kidney injury, because it raises the lifetime risk of chronic kidney disease.

Hydronephrosis

Hydronephrosis is dilatation of the renal pelvis and calyces caused by obstruction to the outflow of urine, which raises the pressure inside the collecting system and, if it is not relieved, flattens the calyces, thins the cortex and destroys nephrons. It is not a diagnosis in itself but a sign that something is blocking the urinary tract, so its whole management is about finding the level of the obstruction and draining the system before function is lost.

The level of the block is read off the pattern: BILATERAL hydronephrosis with a distended bladder means obstruction at or below the bladder outlet — prostate, urethral stricture, posterior urethral valves, a blocked catheter or a pelvic mass — while UNILATERAL hydronephrosis means a block in that ureter or at the pelvi-ureteric junction, most often a stone.
Causes vary with age: in the newborn and infant, pelvi-ureteric junction obstruction is commonest and posterior urethral valves are the important one in boys, with vesicoureteric reflux behind them; in adults it is calculi; in older men benign prostatic hyperplasia; and in women pregnancy and pelvic malignancy such as carcinoma of the cervix.
Hydronephrosis of pregnancy is physiological, is far commoner on the RIGHT because the gravid uterus is dextrorotated and the right ureter crosses the iliac vessels, appears from the middle of the second trimester and resolves after delivery; it needs no intervention unless there is pain, infection or deteriorating function.
Ultrasound is the first investigation and is safe in pregnancy and in children; a non-contrast CT of the kidneys, ureters and bladder is the best test for stones, a micturating cystourethrogram is used in children for reflux and valves, and a diuretic renogram using MAG3 or DTPA distinguishes a truly obstructed system from a merely baggy one and gives the differential function.
Presentation ranges from silent disease found on a scan, through a dull loin ache or classic ureteric colic radiating from loin to groin, to a palpable mass in a child, to complete anuria when both sides are blocked; a slowly obstructing kidney can be destroyed with almost no symptoms at all.
Treatment is to relieve the obstruction — a urethral catheter for bladder outlet obstruction, a retrograde JJ ureteric stent or a percutaneous nephrostomy for an obstructed ureter — followed by definitive treatment of the cause, whether stone removal, prostatectomy, pyeloplasty for pelvi-ureteric junction obstruction, or ablation of posterior urethral valves.
An obstructed and INFECTED kidney, or pyonephrosis, is a urological emergency: fever and rigors with an obstructed system will not respond to antibiotics alone because the drug cannot reach the pus behind the block, so the system has to be drained within hours by nephrostomy or stent.
Post-obstructive diuresis follows relief of a long-standing obstruction, when the kidney pours out large volumes of urine and the patient becomes volume- and electrolyte-depleted: measure the urine hourly, replace roughly half to three-quarters of the loss with the prescribed fluid once the output exceeds about 200 mL/h, weigh daily, and check sodium, potassium and magnesium at least once a day.
After a chronically distended bladder is catheterised, drain it steadily and watch for haematuria and hypotension; the kidney recovers if the obstruction is relieved within days to a few weeks, but a completely obstructed kidney left for months will not.

Pyelonephritis

Acute pyelonephritis is infection of the renal parenchyma and the pelvicalyceal system — an UPPER urinary tract infection — and it presents with fever, rigors and loin pain rather than with the simple dysuria of cystitis. It matters because it is the urinary infection that causes sepsis, that scars kidneys in children, and that in pregnancy precipitates preterm labour and acute respiratory distress, so it is treated as a systemic illness and not as a bladder problem.

The classic picture is fever above 38 degrees Celsius with rigors, loin or flank pain, costovertebral angle tenderness on gentle percussion, nausea and vomiting, with or without the lower tract symptoms of dysuria, frequency and urgency; in an elderly patient it may present only as confusion or a fall.
Escherichia coli causes the large majority of cases, with Klebsiella, Proteus (associated with struvite stones and alkaline urine), Enterococcus and Pseudomonas behind it; hospital-acquired and catheter-associated infections shift both the organism and the resistance pattern.
White cell CASTS in the urine are the finding that localises infection to the renal parenchyma and separate pyelonephritis from cystitis; pyuria, nitrites and leucocyte esterase only say that there is an infection somewhere in the tract.
Urine is sent for culture and sensitivity BEFORE the first antibiotic dose in every case, with blood cultures if the patient is admitted or septic; the specimen is a mid-stream clean catch, and in a catheterised patient it is taken from the sampling port and never from the drainage bag.
Treatment is antibiotics guided by local resistance: hospitalised or severe cases receive an intravenous agent such as ceftriaxone or piperacillin-tazobactam, stepped down to an oral agent once the patient has been afebrile for 24 to 48 hours and the culture is back, with a total course usually of 7 to 14 days. Fluoroquinolone resistance among Indian urinary isolates is high, so they are not a reliable empirical choice here.
Pregnant women with pyelonephritis are admitted and treated intravenously, because it is a leading non-obstetric cause of hospitalisation in pregnancy; fluoroquinolones and tetracyclines are avoided, and asymptomatic bacteriuria is screened for and treated in pregnancy precisely to prevent this illness.
If fever and pain have not settled within 48 to 72 hours of appropriate antibiotics, image the patient: the reasons for failure are an obstructing stone, a renal or perinephric abscess, or emphysematous pyelonephritis, which occurs in poorly controlled diabetics, shows gas on CT and carries a high mortality needing drainage or nephrectomy.
Complications are septic shock, acute kidney injury, renal and perinephric abscess, papillary necrosis (in diabetes, sickle cell disease and analgesic nephropathy) and, in young children, permanent renal scarring seen on DMSA scanning that leads to hypertension and chronic kidney disease later in life.
Nursing care is fluids, antipyresis and observation: maintain hydration so that the urine stays dilute and flowing, record temperature, pulse, blood pressure, respiratory rate and urine output, give analgesia for the loin pain, and teach prevention — 2 to 3 litres of fluid a day, do not delay voiding, wipe from front to back, void after intercourse and complete the whole antibiotic course.

Exstrophy of bladder

Bladder exstrophy is a congenital defect in which the lower anterior abdominal wall and the anterior wall of the bladder both fail to close, so the baby is born with the posterior bladder wall lying exposed on the abdomen and urine dribbling from the two ureteric orifices onto the skin. It sits in the middle of the exstrophy-epispadias complex, between isolated epispadias and cloacal exstrophy, and it is a nursing emergency from the first minute of life because the exposed bladder plate is fragile, the baby loses heat and fluid through it, and what is placed on that mucosa in the delivery room determines whether the bladder can later be closed.

It is rare, of the order of 1 in 30,000 to 50,000 live births, and commoner in boys; the underlying failure is that the cloacal membrane is not reinforced by mesoderm, so it ruptures and the structures in front of the bladder never form.
The findings at birth are a glistening red bladder plate on the lower abdomen with urine visibly jetting from the ureteric orifices, a low-set umbilicus, a wide separation of the pubic bones (pubic diastasis) with outward rotation of the hips, and epispadias — a short penis with the urethral plate on its dorsal surface in boys, and a bifid clitoris with a wide separated labia in girls.
Associated problems are vesicoureteric reflux in almost all cases, inguinal hernias, a waddling or out-toeing gait from the pubic diastasis, and, if the bladder plate stays exposed, squamous metaplasia and later adenocarcinoma.
Immediate care of the plate: cover it with a clear non-adherent plastic wrap (cling film), never with dry gauze, petroleum gauze or any adherent dressing, because gauze sticks to and strips the mucosa; irrigate with warm sterile saline and re-apply fresh wrap at every nappy change.
Tie the umbilical cord with a silk ligature instead of a plastic clamp, because a hard clamp lying against the bladder plate abrades it.
Nurse the baby latex-free from birth — like children with spina bifida, these babies undergo repeated surgery and develop latex allergy at high rates, so gloves, catheters and equipment must all be latex-free and the allergy alert recorded from day one.
General newborn priorities run alongside: keep the baby warm, since heat and fluid are lost through the exposed plate, monitor temperature and fluid balance, position supine or on the side without pressure on the bladder, keep the plate clear of faecal contamination at nappy changes, and start the prescribed antibiotic prophylaxis with a renal ultrasound to look for hydronephrosis.
Surgery is staged: primary bladder and abdominal wall closure in the first 48 to 72 hours of life (later closure needs a pelvic osteotomy to bring the pubic bones together), then epispadias repair in infancy, then bladder neck reconstruction at around 4 to 5 years when the child can take part in toilet training; some centres perform a complete primary repair instead.
After closure the child is immobilised as prescribed, often with lower-limb traction or a spica, the ureteric stents and suprapubic catheter are kept patent and their drainage measured separately, and the wound and the closure are protected from any rise in intra-abdominal pressure — crying, straining or abdominal distension can disrupt it.
Long-term follow-up is for continence, upper tract protection against reflux and infection, clean intermittent catheterisation where needed, fertility and sexual function, and psychological support; the parents need to be told at the outset that the appearance is correctable and that the condition was not caused by anything they did.

Urolithiasis

Urolithiasis is the formation of stones anywhere in the urinary tract when the urine becomes supersaturated with a salt and the inhibitors of crystallisation are outmatched. Its bedside face is ureteric colic — a sudden, severe, cramping loin-to-groin pain in a patient who cannot lie still — and its danger is not the pain but the combination of obstruction with infection, which destroys a kidney within hours and can kill.

Composition and behaviour: calcium oxalate accounts for about 70 to 80% and is radio-opaque; calcium phosphate forms in alkaline urine; struvite (magnesium ammonium phosphate) forms in alkaline urine infected with urease-producing Proteus or Klebsiella and grows into staghorn calculi; uric acid stones are radiolucent on plain X-ray and form in acid urine in gout, high purine intake and after chemotherapy; cystine stones occur in cystinuria and are faintly opaque.
The uric acid stone is the only common stone that dissolves medically — urinary alkalinisation with potassium citrate to a urine pH of about 6.5 with high fluid intake, plus allopurinol where the urate load is high.
The pain distinguishes itself by behaviour: the patient with colic writhes and cannot find a comfortable position, whereas the patient with peritonitis lies absolutely still. Nausea, vomiting, urgency and visible or microscopic haematuria complete the picture, and haematuria is present in most but not all cases.
Non-contrast CT of the kidneys, ureters and bladder is the diagnostic standard and shows every stone type including uric acid; ultrasound is first-line in pregnancy and in children and shows hydronephrosis; a plain X-ray misses radiolucent stones and is used mainly for follow-up of a known opaque stone.
Analgesia is a non-steroidal anti-inflammatory drug first — for example diclofenac by intramuscular or intravenous route — because it relieves renal colic better than an opioid and reduces ureteric wall oedema; an opioid is added or substituted when NSAIDs are contraindicated by renal impairment, bleeding risk or pregnancy. Antispasmodics and an antiemetic are given alongside.
Passage depends on size and site: stones under 5 mm pass spontaneously in about 80 to 90% of cases, 5 to 10 mm in about half, and stones above 10 mm rarely pass. Medical expulsive therapy with the alpha-blocker tamsulosin 0.4 mg once daily helps distal ureteric stones larger than 5 mm and is continued for up to about 4 weeks, with the patient warned about postural dizziness.
Interventions: extracorporeal shock wave lithotripsy for renal and upper ureteric stones up to about 2 cm; ureteroscopy with laser fragmentation for ureteric stones and for those that fail lithotripsy; percutaneous nephrolithotomy for stones above about 2 cm, staghorn calculi and lower pole stones; a JJ stent or percutaneous nephrostomy to relieve obstruction urgently.
Prevention is where the nurse changes the disease: fluid intake of about 2.5 to 3 litres a day aiming for a urine output above 2 to 2.5 litres, reduced salt, reduced animal protein, reduced oxalate-rich foods such as spinach, beetroot, nuts, chocolate and strong tea for oxalate formers, and — the counterintuitive point — a normal dietary calcium intake, because restricting calcium increases oxalate absorption and makes stones more likely.
Metabolic follow-up: strain all urine and send the passed stone for analysis, because the composition dictates prevention; check serum calcium, uric acid, creatinine and electrolytes, and a 24-hour urine in recurrent stone formers; thiazide diuretics reduce hypercalciuria and potassium citrate corrects hypocitraturia.
Complications are obstruction with hydronephrosis and loss of function, recurrent infection, an infected obstructed system (pyonephrosis), and, over years, renal failure in bilateral or staghorn disease.

Urinary incontinence — types

Urinary incontinence is any involuntary leakage of urine, and it is classified by what provokes the leak, because the type decides the treatment far more than the volume does. It is common, under-reported and rarely dangerous in itself, but it causes falls, pressure damage, urinary infection, social withdrawal and admission to institutional care, so identifying the type is one of the highest-value assessments a nurse performs.

Stress incontinence is leakage on coughing, sneezing, laughing, lifting or exercise, with no urge beforehand; it is caused by urethral hypermobility or intrinsic sphincter deficiency after vaginal delivery, multiparity, menopause, obesity, chronic cough or prostatectomy.
Urge incontinence is a sudden desperate need to void with leakage before the toilet is reached, usually with frequency of more than 8 voids a day and nocturia; it is caused by detrusor overactivity and is the incontinence of overactive bladder, stroke, Parkinson disease and bladder irritation.
Overflow incontinence is constant dribbling from a chronically full bladder that never empties, with hesitancy, a poor stream and a palpable bladder; it follows bladder outlet obstruction from benign prostatic hyperplasia or stricture, diabetic or other neurogenic bladder, and anticholinergic drugs. A post-void residual above about 100 to 150 mL confirms it.
Functional incontinence is leakage in a person whose bladder works but who cannot reach or use the toilet in time because of immobility, arthritis, dementia, restraints, poor lighting or a bed too high; mixed incontinence combines stress and urge and is common in older women.
Transient and reversible causes are remembered as DIAPPERS — Delirium, Infection, Atrophic vaginitis, Pharmaceuticals (diuretics, sedatives, alpha-blockers, anticholinergics), Psychological causes, Excess urine output from diabetes or heart failure, Restricted mobility and Stool impaction — and every one of them is checked before a type is labelled.
Assessment: a 3-day bladder diary of intake, voided volumes and leaks, urinalysis and culture to exclude infection, blood glucose, post-void residual by bladder scan, a cough stress test, and in women a pelvic examination for prolapse and atrophy; in men a prostate assessment.
First-line treatment of stress incontinence is supervised pelvic floor muscle training for at least 3 months (a common prescription is 8 contractions three times a day), with weight reduction, treatment of chronic cough and constipation, and topical oestrogen for atrophy; surgery such as a mid-urethral sling or colposuspension follows if training fails, and a pessary helps where prolapse contributes.
First-line treatment of urge incontinence is bladder training with scheduled voiding and gradually lengthened intervals for at least 6 weeks, with caffeine and alcohol reduction; drugs are added second — antimuscarinics such as oxybutynin, tolterodine or solifenacin, or the beta-3 agonist mirabegron, followed by intravesical botulinum toxin or sacral neuromodulation.
The drug cautions are examinable: antimuscarinics cause dry mouth, constipation, blurred vision, urinary retention and, in the elderly, confusion and falls from anticholinergic burden, and they are avoided in narrow-angle glaucoma; mirabegron raises blood pressure and is avoided in severe uncontrolled hypertension.
Nursing care in every type: do not restrict fluids severely, because concentrated urine irritates the bladder and worsens urgency — aim for a normal intake with less in the late evening; offer timed toileting and a call bell within reach, use a barrier cream and pH-balanced cleanser for moisture-associated skin damage, and never use an indwelling catheter for staff convenience, since it exchanges incontinence for catheter-associated infection.

Faecal incontinence

Faecal incontinence is the recurrent involuntary loss of solid or liquid stool, and flatus incontinence is its milder form; continence depends on stool consistency, rectal capacity and sensation, the internal and external anal sphincters and the puborectalis sling, and the intact ability to reach a toilet, so a failure in any one of these produces it. It is grossly under-reported because patients are ashamed to mention it, and in hospital it is the commonest driver of moisture-associated skin damage and pressure ulceration.

Causes in women are led by obstetric anal sphincter injury from third and fourth degree tears, instrumental delivery and prolonged second stage, and the incontinence often appears years later at the menopause when the sphincter reserve is lost.
Other causes: faecal impaction with overflow (the commonest cause in frail, immobile and elderly patients, and a treatable one); neurological disease such as cauda equina syndrome, spinal cord injury, multiple sclerosis, stroke, dementia and diabetic autonomic neuropathy; diarrhoeal disease including inflammatory bowel disease and irritable bowel syndrome; rectal prolapse and haemorrhoids; and previous anorectal surgery such as fistulotomy or haemorrhoidectomy.
Assessment starts with a bowel diary and Bristol stool chart, then abdominal examination, digital rectal examination for impaction, resting tone (internal sphincter) and squeeze pressure (external sphincter), perianal sensation and the anal wink reflex, and inspection for prolapse, soiling and excoriation.
Investigations when the cause is not obvious: endoanal ultrasound to show a structural sphincter defect, anorectal manometry with sensation testing, defaecography for prolapse or obstructed defaecation, and colonoscopy where there is bleeding, weight loss or a change in bowel habit.
Overflow from impaction is confirmed by a loaded rectum on examination with a history of leaking liquid stool in a constipated patient — the treatment is disimpaction and then a regular bowel regimen, and giving a constipating drug such as loperamide at this point makes it much worse.
Conservative management works in most patients: firm the stool with soluble fibre such as ispaghula and by treating the diarrhoea, use loperamide 2 mg titrated and taken before meals or before going out, empty the bowel predictably by toileting 20 to 30 minutes after a meal to use the gastrocolic reflex, and add pelvic floor exercises with biofeedback, which is the most effective non-surgical treatment.
Skin care is a nursing priority in its own right: cleanse with a pH-balanced no-rinse cleanser rather than soap and hot water, pat dry without rubbing, apply a barrier film or cream at every episode, use breathable absorbent products changed promptly, and inspect the perineum, natal cleft and buttocks at every change for moisture-associated damage that will otherwise become a pressure ulcer.
Surgery and devices are for those who fail conservative care: an anal plug, sacral nerve stimulation, sphincteroplasty for a defined obstetric defect, injectable bulking agents, and a stoma as the last option, which for some patients is a liberation rather than a defeat.
Pads and containment are never a substitute for a toileting programme; the plan should aim at planned, controlled evacuation, and continence products are the safety net around it.
Prevention and dignity: identify and repair obstetric tears at delivery, keep hospitalised patients mobile and their bowels regular, review constipating and laxative drugs, provide privacy and prompt response to the call bell, and record the conversation in the patient's own words so she does not have to raise it again.

Urinary tract infection (UTI)

Urinary tract infection is bacterial invasion of the urinary tract, and it is divided into lower tract infection (cystitis and urethritis, with dysuria, frequency, urgency and suprapubic pain but no systemic upset) and upper tract infection (acute pyelonephritis, with fever, rigors, loin pain and vomiting). It is called uncomplicated in a non-pregnant woman with a structurally normal tract and complicated when it occurs in pregnancy, in men, in children, with a catheter, with obstruction, stones, diabetes or immunosuppression — a distinction that changes the investigation, the drug and the duration.

Escherichia coli causes about 75 to 85% of uncomplicated infections; Staphylococcus saprophyticus occurs in sexually active young women, Proteus (a urease producer, alkaline urine, struvite stones) and Klebsiella in complicated infection, and Enterococcus, Pseudomonas and Candida in catheterised and hospitalised patients.
Women are affected far more often because the urethra is short and close to the anus; other risk factors are sexual intercourse, spermicide and diaphragm use, pregnancy, menopausal oestrogen deficiency, diabetes, incomplete bladder emptying, stones and catheterisation.
Significant bacteriuria is classically 100,000 colony-forming units per mL of a single organism in a clean-catch midstream sample, but a much lower count is meaningful in a symptomatic woman, and any growth from a suprapubic aspirate counts; the specimen must reach the laboratory within an hour or be refrigerated.
Dipstick: nitrite is highly specific because it needs nitrate-reducing Enterobacteriaceae and several hours of bladder incubation, so a positive nitrite is nearly diagnostic while a negative one does not exclude infection; leukocyte esterase is sensitive but not specific. Sterile pyuria points to tuberculosis, chlamydia, stones, a partially treated infection or analgesic nephropathy.
Uncomplicated cystitis is treated with nitrofurantoin 100 mg twice daily for 5 days, or fosfomycin 3 g as a single dose, or co-trimoxazole where local resistance is low; fluoroquinolones are avoided for simple cystitis because of resistance and tendon and neurological toxicity, and nitrofurantoin is avoided in significant renal impairment and at term in pregnancy.
Acute pyelonephritis needs urine and blood cultures and 7 to 14 days of treatment, starting intravenously with a third-generation cephalosporin such as ceftriaxone in an unwell patient; if the fever has not settled in 48 to 72 hours, image the tract for obstruction, an abscess or emphysematous pyelonephritis in a diabetic.
Asymptomatic bacteriuria is treated only in pregnancy and before urological procedures that breach the mucosa; it is deliberately not treated in the elderly, in residents of care homes or in catheterised patients, where treatment causes resistance and Clostridioides difficile without benefit. This stewardship rule is the most commonly examined discriminator in this topic.
In pregnancy every woman is screened with a urine culture in early pregnancy, because untreated asymptomatic bacteriuria progresses to pyelonephritis in a substantial proportion and is associated with preterm birth and low birth weight; safe choices include cefuroxime, amoxicillin-clavulanate and nitrofurantoin except at term, while fluoroquinolones and tetracyclines are avoided throughout.
In children under 2 years the infection presents as fever without a focus, vomiting, poor feeding, irritability or failure to thrive, so urine must be collected before antibiotics are started and an ultrasound arranged, with further imaging for recurrent or atypical infection to look for vesicoureteric reflux and renal scarring.
Catheter-associated infection is prevented, not treated: insert a catheter only for a valid indication, use aseptic technique, keep the drainage system closed with the bag below the level of the bladder and off the floor, secure the catheter, avoid routine bladder washouts and prophylactic antibiotics, review the need daily and remove it at the earliest opportunity.
Self-care advice that reduces recurrence: fluid intake of about 2 to 3 litres a day, do not delay voiding, void after intercourse, wipe from front to back, avoid spermicides, and consider vaginal oestrogen after the menopause; the evidence for cranberry products is weak.

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