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Chapter4
Fluids andrenal
Acute kidney injury 394
Chronic kidney disease 395
Haematuria 396
Proteinuria 397
Glomerular disease 398
Urological disorders 399
Low urine output 400
IV uids 402
2Potassium emergencies 406
Electrolyte imbalance 407
393
394 CHAPTER4 Fluids andrenal
Acute kidneyinjury
$ Decline in renal function over hours or days, with failure to maintain
uid, electrolyte, and acid–base homeostasis (Box 4.).
There are three basic mechanisms:
Prerenal Hypoperfusion of kidney due to eg dBP, hypovolaemia,
sepsis, haemorrhage, renal artery occlusion (mass, emboli).
RenalIntrinsic renal pathology, eg glomerulonephritis, vasculitis,drugs.
PostrenalObstruction of outow tract (ureter, bladder, urethra) by eg en-
larged prostate, single functioning kidney with calculi, pelvic mass, or surgery.
Acute tubular necrosis is irreversible renal damage with nephron loss that
may occur due to prerenal or renal triggers, eg prolonged hypoperfusion
or nephrotoxins (eg NSAIDs, gentamicin, IV contrast).
3Call for
senior helpearly and discuss with nephrology if concerned.
History Previous renal or other medical problems, urine output, uid
intake, medications (?nephrotoxic), rashes, bleeding, lethargy, anorexia.
2Box 4. Features ofdierent types ofkidneyinjury
Prerenal
hypoperfusion
Acute tubular
necrosis
Renal
Obstruction Oligo/ anuria, hydronephrosis on USS urinary tract; if
Chronic kidney
disease
Oliguria, urine osmolality >500mOsmol/ kg, urine Na+
<20mmol/ L
Oliguria/ normal/ polyuria, urine osmolality <350mOsmol/
kg, urine Na
Oligo/ anuria, haematuria, iBP
urethral:painful anuria with palpable bladder
Oliguria/ normal/ polyuria, previous icreatinine, dHb, dCa2+,
iPO
2
+
>40mmol/ L
3−
, small kidneys on USS, fatigue, nocturia
4
2
Examination Volume status (E p. 402), BP (compare to what is
normal for patient from eg old observation charts or GP records), HR,
JVP, basal creps, oedema, palpable bladder, rashes, masses.
Investigations UrineColour, hourly volume, dipstick, M,C+S, osmo-
lality and Na
ESR, clotting;
+
(E pp. 596–7);bldsFBC, U+E, LFT, CK, CRP, osmolality,
ABGBeware acidosis or iK
+
; 2Urgent ECG iK+ causes at
P waves, wide QRS, and tall, peaked T waves;
Urinary tractUSS
TreatmentUrinary catheter (E pp. 574–5) to monitor output. Continue
IV uids unless overloaded (no KCl if iK
To identify obstruction or renal artery stenosis.
+
), review medication doses, stop
nephrotoxins (E p. 70), eg ACEi/ARB, metformin, diuretics, NSAIDs.
Assess for, and treat, the cause(s) and complications;
will relieve urethral obstruction; ureteric obstruction may require
nephrostomy or stenting. Discuss with urology team;
sent JVP; uid resuscitate (E pp. 478–9) ±inotropes. Discuss with HDU/
ITU/tertiary renal unit;
osemide (E p. 199),CXR;
salbutamol (Ep. 407);
May be dened as any of:icreatinine of ≥26micromol/ L in ≤48h, or ≥50% in 7d (if recent bloods unavailable consider
baseline values plus clinical history);
2
In prerenal states, the hypoperfused kidney attempts to conserve water and electrolytes, passing waste
solutes as a maximally concentrated urine low in sodium. With tubular necrosis, concentrating ability is lost.
Overloaded Oedema, basal creps, iJVP: O
HyperkalaemiaInsulin/ glucose, Ca
Intrinsic renal cause Involve nephrologist early.
or
durine output <0.5mL/ kg/ h for >6h; M https://www.nice.org.uk/guidance/ng48
CXR Pulmonary oedema
Obstructed Catheter
Shocked iHR, dBP, ab-
2
2+
gluconate,
, fur-
Chronic kidney disease
$ Long- standing and irreversible reduction inGFR.
Causes DM, iBP, AKI,
pyelonephritis, polycystic kidneys, vasculitis, nephrotoxic medications.
4
chronic urinary obstruction, glomerulonephritis,
SymptomsInitially none; tiredness, weight loss, nausea, loss of taste.
SignsInitially none, may have signs of the causative disease,egDM.
Results iurea, icreatinine, deGFR, dHb, dCa
ratio (ACR E p. 619), persistent haematuria, abnormal/ small kidneys on USS;
consider biopsy if cause unclear.
MonitoringAt least annually, more frequently in severe disease; blds FBC, U+Es,
2
eGFR, Ca
Treatment Address risk factors Tight BP
control (<40/90mmHg, if ACR >70mg/
mol <30/80mmHg), DM, smoking cessation, avoidance of nephrotoxins, reduction of
CVD risk;
improves proteinuria and BP (avoid initiating
+
if K
>5mmol/L, stop if K+ >6mmol/L).
Consider nephrology referral, eg for G4/G5
disease, ACR >70mg/mmol (or >30mg/
mmol with haematuria), progressive eGFR
decrease, or suspected rare/genetic cause;
Management of complications Includes cor-
rection of anaemia with iron replacement
±erythropoietin, dietary modication, and
oral Ca2+ supplements/PO
prevent dCa2+/ iPO
hyperparathyroidism with vitamin D analogues. As patients near end- stage disease
(Table 4.), discuss wishes and suitability for dialysis (Box 4.2) or transplantation, and make necessary arrangements (eg dialysis counselling, stula creation).
Complications Vascular disease, anaemia, dCa
iK+, uid overload, immune compromise, peripheral neuropathy.
Prescribing E p. 70; avoid nephrotoxic drugs (eg metformin, NSAIDs,
gentamicin); reduce doses/ frequency of renally excreted drugs (eg opioids,
benzodiazepines, penicillins); see also E pp. 402–5 for uids.
Radiology Avoid IV contrast imaging except in an emergency since this is
nephrotoxic; discuss carefully with nephrology and radiology. Where essential,
use IV hydration and monitor renal function closely.
3–
+, PO
;
Urine for ACR.
4
ACEi/ARB Titrated to highest dose
3–
binders to
4
3–
, control of secondary
4
T Box 4.2 Patients ondialysis
Approximately 5,000 UK patients are on haemodialysis, usually for 3– 5h 3×/
week via an arteriovenous stula. Blood tests and BP measurements should never
be made from a stula arm. Placing ngers or a stethoscope bell gently over a
stula will conrm function if a gentle buzz is felt or heard. Afurther 5000 UK
patients use peritoneal dialysis via an abdominal (Tenckho) catheter. Peritoneal
infections in these patients can be devastating; if septic, a sample of dialysate
should be inspected (?turbid) and sent for cell count, Gram stain, and culture;
intraperitoneal antibiotics may be required. Always inform the renalteam.
3
NICE guidelines available at Mhttps://www.nice.org.uk/guidance/ng203 See also the UK renal
association website Mhttps://ukkidney.org/ for useful educational material andlinks.
4
Patients with AKI should have monitoring for development or progression of CKD for at least
3yr, even if eGFR has returned to baseline.
3
2+
3–
, iPO
, ialbumin:creatinine
4
Table4. CKD classication
eGFR (mL/ min) Stage
>90 G
60– 89 G2
45– 59 G3a
30– 44 G3b
5– 29 G4
<5 G5 (ESRF)
Reduction in eGFR needs to be
sustained >90d. Combine eGFR
categories with ACR category
(A<3mg/ mmol; A2 3– 30mg/ mmol,
A3>30mg/ mmol) for full classication.
2+
, renal osteodystrophy,
395CHRONIC KIDNEY DISEASE
396 CHAPTER4 Fluids andrenal
Haematuria
2Worrying features Weight loss, frank blood, or clots (?malig-
nancy); iBP, proteinuria (?nephritic syndrome Ep. 398).
Think about Macroscopic UTI, tumours, stones; Microscopic with red
UTI, bladder, renal or prostate tumour, stones, recent catheteriza-
cells
tion, glomerulonephritis/ nephritic syndrome, endocarditis, clotting abnormality, sickle cell, TB, schistosomiasis, trauma, strenuous exercise,
PV bleeding (E pp. 526–9);
globinuria) haemolytic anaemia, myositis, rhabdomyolysis, trauma, ischaemia;
Red discolouration Rifampicin, beetroot.
Ask aboutUrine colour and volume, clots, dysuria, frequency, urgency,
fever, abdominal pain, hesitancy, poor stream, recent trauma or catheterisation, weight loss, malaise, lethargy, menstruation;
disease, stones, prostate disease, cancer, clotting disorders, sickle
cell;
DH Nephrotoxic drugs (eg NSAIDs, gentamicin), rifampicin,
anticoagulants.
ObsBP, HR, temperature, uid balance.
Look for iBP, haematuria, and proteinuria suggest nephritic syndrome
(E p. 398); inspect the urine; rashes, bruises, splinter haemorrhages,
palpate for suprapubic or loin tenderness or masses; PR:enlarged prostate; PV bleeding.
Investigations UrineDipstick may not distinguish red cells and haemo-
globin, microscopy (for red cell or protein casts), culture;
2+
LFT, Ca
ANCA, ANA, anti- DNA), complement, PSA;
, ESR, CRP, clotting; consider G+S, autoantibodies (anti- GBM,
Management Macroscopic(Red/ pink urine.) Resuscitate (E p. 482), if
heavy consider inserting a three- lumen/way catheter for bladder washouts, discuss with urology to exclude malignancy (IVU, cystoscopy,CT);
Microscopic(urine looks normal, red cells on dipstick or microscopy):
•
With nitrites/ white cells Treat as a UTI/ pyelonephritis (E p. 488), check
urine once infection has cleared to be sure haematuria has resolved
•
Without proteinuria This suggests urological tumour or stones (E p. 309),
refer to urology (urgently if >50yr) for CT- KUB ±cystoscopy
•
With proteinuria This suggests glomerular pathology, refer to nephrology
and check BP, urinary output, urine casts, autoantibodies, complement,
urine protein:creatinine, 24h urine collection for protein, renalUSS.
HaemoglobinuriaHaemolytic anaemia (E p. 416), rhabdomyolysis (Box4.3).
K Box 4.3 Rhabdomyolysis
First described in crush victims during the Blitz, this involves muscle
necrosis after crush injuries or after lying on a hard surface for prolonged periods (eg elderly patients who fall and are unable to get up).
Myocyte contents are nephrotoxic and lead to renal failure with iii CK
(but normal troponins), with haemoglobinuria. Treatment is as for AKI
(E p. 394), with management of hyperkalaemia (E p. 407) ± surgical
debridement.
Microscopic without red cells (i.e. haemo-
bldsFBC, U+E,
USSUrinarytract.
PMH Kidney
Proteinuria
2Worrying features iBP, oliguria, haematuria, ii protein, oedema.
Think about Transient Physical exertion, fever, UTI, vaginal discharge,
recent ejaculation;
Primary renal disease Glomerulonephritis; Multisystemic disease Vasculitis,
lupus, endocarditis, myeloma, hepatitis C, pre- eclampsia.
Ask about Recent exercise, vaginal discharge, pregnancy, dysuria, frequency,
urgency, urine output, fever, haematuria, arthralgia or rash, malaise, lethargy,
oedema, orthopnoea, recent URTI/ tonsillitis;
disease, cholesterol, DM;
ObsBP, HR, RR, temp, uid balance, blood glucose.
Look for Evidence of the underlying pathology: oedema, basal creps,
iJVP, suprapubic or loin tenderness, palpable kidneys or uterus, rashes/
arthralgia, splinter haemorrhages.
Investigations Urine Dipstick (protein, blood, nitrites, leucocytes; re-
peat early in morning to exclude postural proteinuria), check β- hCG,
microscopy (for casts), culture, electrophoresis, spot albumin:creatinine
ratio— a more practical initial investigation than a 24h collection for
protein (E p. 619);
antibodies (anti- GBM, ANCA, ANA, anti- DNA), complement, cryoglobulins, serum electrophoresis;
Diagnosis and management
• Fever/ exercise/ transient Repeat urine dipstick normal, no treatment
•
Orthostatic Age <30yr, no protein in early morning, no treatment
•
UTI Dysuria, frequency, urine nitrites/ leucocytes, culture +ve (Ep. 488)
•
Pre- eclampsia Pregnancy, iBP ±oedema (Ep. 501)
•
Myeloma >60yr, bone pain, urine Bence Jones protein, iCa
•
Nephrotic syndrome Oedema, dalbumin, itriglycerides (Ep. 398)
•
DM Tight glycaemic and BP control, ACEi (Ep. 344)
•
Tumour lysis syndrome See Box 4.4.
K Box 4.4 Tumour lysis syndrome
The destruction of malignant cells during chemotherapy causes release of
intracellular contents which may overwhelm renal elimination and extracellular buers; the resulting metabolic derangement, together with the
precipitation of uric acid crystals within the tubules, can cause AKI. Risk
factors include pre- existing renal impairment with high- grade tumours,
lymphoma, or leukaemia. Onset is generally within 3d of chemotherapy,
with oliguria, muscle cramps, tingling, weakness, tetany, and seizures.
Blood tests will show iK
Treatment
Involves recognition of at- risk patients and prophylactic IV hydration and allopurinol started 24– 48h prior to therapy with careful monitoring of electrolytes during therapy. If the syndrome still develops, attempt
hyperhydration with IV uids, allopurinol (or rasburicase if high risk), bicarbonate, K+ restriction, and
Dialysis may be necessary to prevent worsening renal failure, refractory
hyperkalaemia, and ultimately arrhythmias and cardiac arrest.
Extrarenal causes Orthostatic, hypertension, LVF;
DHNephrotoxic drugs (eg NSAIDs, gentamicin).
blds FBC, U+E, LFT, triglycerides, ESR, CRP, auto-
+
3−
, iPO
4
3−
PO
binding under advice from the renal team.
4
PMHKidney disease, iBP, heart
USSKidneys/ urinarytract.
2+
(Ep. 411)
, dCa2+, iurate, iurea, icreatinine.
397PROTEINURIA
398 CHAPTER4 Fluids andrenal
Glomerular disease
$ A spectrum of diseases aecting glomerular capillaries, mesangial cells,
and/or podocytes, often causing leakage of proteins or blood into the urine.
Nephrotic syndrome
Dened as >3.5g proteinuria/ 24h with hypoalbuminaemia (<30g/L) and
oedema. Hypercholesterolaemia, dIgG, and hypercoagulability may also feature. Causes include primary glomerulonephritis as below (typically minimal
change or membranous disease) but also extra renal causes including DM,
anti- GBM disease, malaria, pre- eclampsia, and drugs (eg gold, penicillamine,
NSAIDs). Treatment is of the underlying cause, alongside diuretics, active
treatment of infection, and VTE prophylaxis.
Nephritic syndrome
Characterized by iBP, oliguria, and haematuria. This may classically be seen
around 3wk after a streptococcal throat infection as a self- resolving glomerulonephritis, but is also associated with some much more aggressive pathologies including vasculitis and anti- GBM disease.
Glomerulonephritis
$ Inammation of the glomeruli triggered by an immunologic mechanism
results in tissue damage, often with proliferation of basement membrane,
mesangial cells, or capillary endothelium.
Some important histological types and associated causes and clinical features are listed in Table4.2.
Table4.2 Classication ofglomerulonephritis
Biopsy Presentation Causes Management
Minimal
change
(normal
by light
microscopy)
Membranous Heavy proteinuria
Focal
segmental
glomerulosclerosis
Mesangioproliferative
Crescentic Nephritic; rapidly
Nephrotic syndrome
(commonest cause
in children)
±nephrotic
syndrome
Proteinuria
±haematuria and
hypertension
syndrome; CRF
Haematuria (often
<72h after URTI);
nephritic syndrome
progressive to
ESRF
Most idiopathic,
consider drugs
(NSAIDs) or
lymphoma in
adults
Primary (70%;
PLAR2 antibodies in
most) or secondary
(malignancy,
connective tissue
disease, drugs,
hepatitis)
Idiopathic or
genetic; secondary
causesinclude
heroin abuse
andHIV
Idiopathic IgA
deposition
ANCA vasculitis,
anti-GBM disease,
lupus nephritis
Majority steroid
responsive; very few
progress to ESRF
⅓ stabilize with
immunosuppression;
⅓ remit spontaneously;
⅓ progress to ESRF
Primary disease may
respond to steroids but
signicant progression to
ESRF; secondary disease
managed with ACEi
Majority self- limiting but
20– 40% progress to
ESRF; ACEi ±steroids
Immunosuppression,
plasma exchange in
vasculitis
Urological disorders
3Acute urinary retention
Causes Enlarged prostate, postoperative, pain, anticholinergics, spinal
pathology/ MS (painless), pregnancy, constipation,UTI.
SymptomsSuprapubic pain + urge to urinate, anuria/ oliguria, delirium.
SignsPalpable distended bladder (dull to percussion and tender), check
leg power/ reexes and tone, perianal sensation, and prostateonPR.
InvestigationsBladder scan if unsure, or pass a urinary catheter.
Management 2Urgent catheterization (E p. 574), record residual urinary
volume (normal bladder is 400– 500mL, consider acute- on- chronic retention
if >L); urine dipstick and send for M,C+S; stool chart ±laxatives; urgent MRI
spine if new lower limb neurology and diminished perianal sensation/ tone
(E p. 369). Beware post- obstructive diuresis:pay attention to uid balance
and electrolytes. Once reversible causes addressed, attempt a TWOC with
close monitoring for recurrence of retention. If this occurs, reinsert catheter
and treat as chronic retention. Discuss with urology.
ComplicationsAKI, chronic obstruction, chronic retention, UTIs.
Chronic urinary retention
CausesObstruction (prostate), DM, MS, dysfunctional bladder.
SymptomsIncontinence, dribbling, poor stream, recurrentUTIs.
SignsPalpable distended bladder (usually non- tender), large prostate.
Investigations bldsFBC, U+E, PSA, Ca
Management Do not catheterize unless in pain or anuric (acute-on-
chronic retention); refer to urology to investigate cause; options include
TURP, intermittent self- catheterization, anti- androgens (eg nasteride),
or α- blockers (eg tamsulosin).
ComplicationsCKD, recurrentUTIs, urinary strictures.
Urinary incontinence
Types of incontinence:
•
Stress Leakage on exercise/ coughing/ laughing
•
Urge Severe and sudden urgency (often due to detrusor instability)
•
Overow Urine volume exceeds bladder capacity (eg chronic retention)
•
Functional Restricted mobility so unable to get to toilet intime.
Causes UTI, detrusor instability, neurological problem (eg MS, DM), di-
uretics + reduced mobility; ♀:uterine prolapse, weak pelvic muscles,
pelvic mass; ♂:post- prostate surgery.
Ask aboutUrgency, frequency, leakage, dysuria, poor stream, haematuria,
uid intake (including caeine consumption late in the day), eects on
lifestyle, obstetric history, and previous pelvic surgery or trauma, DM,
chronic cough, faecal incontinence. If acute presentation with new leg
weakness, suspect spinal cord compression (Ep. 369).
Look forAbdo/ pelvic masses, prolapse (E pp. 54–5); ?leak on coughing.
Investigations Urine MSU, glucose, urinary diary, urodynamics studies.
♂:
bldsPSA (take prior to checking prostate size and nodularity byPR).
Treatment General Weight loss, less caeine, stop smoking, treat pro-
lapse;
Stress incontinence Fluid restriction, pelvic oor exercises, sur-
gery;
Detrusor instability Bladder training, antimusarinic; Overow See
‘Chronic urinary retention’ earlier in this topic;
2+
3−
,PO
.
4
FunctionalAid mobility.
399UROLOGICAL DISORDERS
400 CHAPTER4 Fluids andrenal
Low urineoutput
2Worrying features Low urine output <0.5mL/ kg/ h (Table4.3)
sustained >4h or despite adequate uid, iHR, systolic BP <00mmHg,
+
iK
, icreatinine, acidosis.
3Do not ignore patients with very low urine output, they will be among
the sickest in the hospital.
than AKI, although patients with underlying CKD and LVF will need
your closest attention for regular review and uid management.
Table4.3 Classication oflow urine output
Normal urine output >60mL (>mL/ kg) >600mL
Low urine output <30mL (<0.5mL/ kg) <800mL
Oliguria <7mL <400mL
Anuria <4mL <00mL
Absolute anuria None None
*Volumes are dened for adult patients; paediatric values are based upon weight.
Think about SevereAKI, shock;Most likelyHypovolaemia, hypotension, urinary
retention, blocked catheter, prostatic hypertrophy;
renal vascular problems (eg thrombosis, emboli), urethral trauma.
Ask about Abdominal pain, hesitancy, poor stream, uid balance (oral
and IV intake, vomiting, diarrhoea, stoma output, leaking wounds, fever/
sweating), breathlessness, orthopnoea, postural dizziness;
disease, solitary functioning kidney, prostate disease, iBP, heart disease,
DM;
DHNephrotoxic drugs (eg NSAIDs, gentamicin, ACEi, IV contrast).
ObsBP, HR, RR, uid balance, CVP if possible.
Look for Volume status (E p. 402), oedema, unrecorded leakage from
wounds, stomas, or surgical drains; palpable bladder, suprapubic pain, loin pain,
enlarged prostate, evidence of infection or haemorrhage.
Investigations UrineColour, dipstick, M,C+S; septic screen, if not responding
to uid challenges call for senior help and send urine for osmolality (E p. 619)
+
and Na
;blds FBC, U+E, CK, osmolality;Bladder scanIf retention or a blocked
catheter is suspected;
causes, request a doppler USS if renal artery stenosis/ embolism is suspected.
Treatment Insert a urinary catheter (E pp. 574–5) and ask the nurses
to keep an hourly uid balance including any diarrhoea, vomiting, and uid
loss from wounds. Consider asking for a catheter ush if already catheterized.
Assess the patient and if in doubt treat as hypovolaemia with a uid challenge
(eg 500mL 0.9% saline over 0– 5min E p. 403) and review in – 2h. Beware
post- obstructive diuresis if in retention/ blocked catheter.
If urine output is still low despitetreatment Then get further senior advice. If a patient
is volume depleted, it may need considerable uid volumes to improve output,
but assess frequently for volume overload. Always rule out urinary tract obstruction. Indiscriminate use of IV furosemide simply to improve output may make the
uid balance chart look better, but does nothing good for your patient.
$ It is usually easier to treat uid overload
*
Volume in h Volume in 24h
Other Rhabdomyolysis, CKD,
USS renal tract Will allow full assessment for structural
PMH Kidney
Table4.4 Common causes oflow urineoutput
History Examination Investigations
Hypovolaemia
(E p. 401)
Septicshock
(E p. 484)
Acute kidney
injury
(E p. 394)
Chronic kidney
disease
(E p. 395)
Urinary
retention
(E p. 399)
Low uid input,
excess losses,
post- op
Malaise, symptoms
of infection, acute
illness
Severe illness,
untreated low urine
output
iBP, lethargy,
anorexia, previous
kidney problems,
DM
Lower abdominal
pain, previous
prostate problems
Negative uid
balance, iHR, dJVP,
±dBP (postural)
iHR, dBP, fever,
iRR, exclude
haemorrhage
May be dehydrated
or shocked
Pale, anaemic,
oedema, bruising,
peripheral
neuropathy
Palpable bladder,
often anuric,
enlarged prostate
iurea, concentrated
urine, iurine
osmolality
May have idWCC,
iCRP, ±ilactate
New- onset iurea
and creatinine, iCK
if rhabdomyolysis
Persistent iurea
and creatinine, small
kidneys on USS
Full bladder on
scan, relief on
catheterization
Hypovolaemia
$ This is by far the most common cause of low UO in in patients.
Symptoms, signs, investigationsSee Table4.4 (see also Box4.5).
Treatment Increase uid input; the rate of rehydration depends on the pa-
tient. If urine output is >0.5mL/ kg/ h simply increase the rate of current IV
uids. If <0.5mL/ kg/ h consider a uid challenge (E p. 403) and prescribe
some quick uids to follow, eg 0.9% saline L/ 4h; review the patient in– 2h.
ComplicationsAKI.
Fluid overload
$ Prescribing of uid volumes that exceed the ability of the kidneys to
excrete may lead to iatrogenic uid overload (eg failure to identify obstructive uropathy or cardiac failure as cause of low output).
Symptoms, signs, investigations(Ep. 402.)
Treatment(E p. 296 ‘Pulmonary oedema’.) For mild overload reduce or
stop IV uids and review in a few hours; ask the nurses to record hourly
obs and contact you if the patient ’s RR rises. If you are certain of overload,
ensure no evidence of obstruction before trying 40mg furosemide IV. This
will cause a diuresis in most patients, but potentially contribute towards AKI
if the patient was hypovolaemic. In certain settings (eg sepsis + cardiogenic
shock) the patient may be intravascularly volume depleted, but symptomatically uid overloaded— this requires senior assessment for HDU/ ICU and
consideration of inotropic support.
ComplicationsPulmonary oedema.
401LOW URINE OUTPUT
I Box 4.5 Causes oflow urine output covered elsewhere
Hypotension/ shock E pp. 476–7 Cardiac failure E p. 282
402 CHAPTER4 Fluids andrenal
IVfluids
Assessing volumestatus
$ HR, postural hypotension, and low urine output (<0.5mL/ kg/ h) are
sensitive signs of hypovolaemia while orthopnoea suggests overload.
Table4.5 Assessing volumestatus
History Examination Investigations
Mild–
moderate
uid decit
(eg <500mL
in adult)
Severe
hypovolaemia
(as for mild
plus…)
Fluid
overload
*Including upper range of normal, ie >90/ min; remains slow if taking β- blockers or other ratelimiting drugs (eg verapamil, diltiazem, digoxin).
is signicant.
durine output,
headache, thirst or
poor oral intake,
excessive uid
loss (eg diarrhoea,
vomiting)
Drowsy, obtunded Oliguria/
Cardiac history,
excess uids, SOB,
orthopnoea, cough,
sputum (white/
frothy), swelling
‡
Ankles if sitting, sacrum if inbed.
iHR,* postural BP
†
drop,
urine output
<0.5mL/ kg/ h, dry
mucous membranes,
capillary rell >2s,
dJVP
anuria, dBP
<00mmHg, sunken
eyes, decreased skin
turgor
iRR, dO
sats, iJVP,
2
bilateral basal crackles,
pitting oedema,
gallop rhythm (3rd
heart sound)
†
A drop of >20mmHg systolic/ 0mmHg diastolic
Fluid balance This is calculated by measuring a patient’s urine output and
uid input along with any losses from vomit, diarrhoea, or drains. The
patient must be catheterized for accurate measurement.
Insensible losses These are unrecordable uid losses, eg sweating and
breathing. 500– 000mL is usually lost each day, but this increases with
pyrexia (from sweating), tachypnoea, and burns; this loss will not be apparent from the uid chart. Litres of uid can be lost from burns and
wound seepage which is missed unless the bandages are inspected.
Third- space uids Also called ‘uid sequestration’; inammation and in-
jury causes capillary permeability to increase so that uid and protein
leak from the blood vessels (intravascular space) causing oedema. The
patient is intravascularly hypovolaemic despite normal uid balance and
uid should be replaced according to clinical signs, especially urine output.
It is common in sepsis, pancreatitis, and after major surgery.
CVP lines Central venous pressure measurements are used primarily in
ICU and HDU since they require a central line (E pp. 562–3). By recording the pressure in the line at the level of the right atrium, an estimate
of lling state is obtained. The normal range is – 7mmHg (– 9cmH
high pressure suggests uid overload or heart failure while a low CVP suggests hypovolaemia. Trends are more important than absolute values; the
CVP should rise with a uid challenge; hypovolaemia has been corrected
once this rise persists after the challenge has nished, or when there is no
further rise in CVP with subsequent uid challenges.
5
NICE guidelines for IV uid prescribing for adults can be found at Mnice.org.uk/guidance/cg74
Dark urine,
iurine osmolality;
blds:iurea,
iPCV/ haematocrit,
ialbumin, iserum
osmolality
icreatinine
Pulmonary oedema
on CXR (E p. 610),
‡
abnormal ECG (E
p. 600— LVH, MI),
iCVP
5
O);
2