catheter for bladder wash-out, discuss with urology to exclude malignancy (IVU, cystoscopy, CT). Microscopic (urine looks normal, red cells on microscopy): \200 With nitrites/white cells treat as a UTI/pyelonephritis (b p484), check urine once infection has cleared to be sure haematuria has resolved Without proteinuria suggests urological tumor or stones (b p295), refer to urology (urgentl y if >50yr) for IVU/CT-KUB cystoscopy With proteinuria suggests glomerular pathology, refer to nephrology and check BP, urinary output, urine casts, autoantibodies, complement, urine pro tein:creatinine, 24h urine collection for protein, renal USS. Haemoglobinuria haemolytic anemia (b p394), rhabdomyolysis (see box). Rhabdomyolysis First described in crush victims during the Blitz, this involves muscle necr osis after crush injuries or after lying on a hard surface for prolonged periods (eg elderl y patients who fall and are unable to get up). Myocyte contents are nephrotoxic and lead to renal failure with iiiCK (but normal troponins), with haemoglobinuria. Treatment is as for acute renal failure (b p372), with man- agement of hyperkalaemia (b p384) surgical debr idement. OHFP.indb 374 OHFP.indb 374 30/05/2014 16:18 30/05/2014 16:18 375 PROTEINURIA Proteinuria Worrying features iBP, oliguria, haematuria, iiproteinuria, oedema. Think about transient physical exertion, fever, UTI, vaginal discharge, recent ejaculation; extra-renal causes orthostatic, hypertension, CCF; primary renal disease glomerulonephriti s; multisystemic disease vas- culitis, lupus, endocarditis, myeloma, hepatitis C, pre-eclam psia. Ask about recent exercise, vaginal discharge, pregnancy, dysuria, frequency, urgency, urine output, fever, haematuria, arthralgia or rash, malaise, lethargy, oedema, orthopnoea , recent URTI/tonsillitis; PMH kidney disease, iBP, heart disease, cholesterol, DM; DH neph rotoxic drugs (eg NSAIDS, gentamicin). Obs BP, HR, RR, temp, fl uid balance, blood glucose. Look for evidence of the underlying pathology: oedema, basal creps, iJVP, suprapubic or lo in tenderness, palpable kidneys or uterus, rashes/ arthralgia, splinter hemorrhages. Invest igations urine dipstick (protein, blood, nitrites, leucocytes; repeat early in morning to e xclude postural proteinuria), check B-hCG, microscopy (for casts), culture, electrophoresis , spot albumin:creatinine ratio \200\223 a more practical initial investigation than a 24h collection for protein (b p591); blds FBC, U+E, LFT, triglycerides, ESR, CRP, autoan- tibo dies (anti-GBM, ANCA, ANA, anti-DNA), complement, cryoglobu- lins, serum electrophoresis; U SS kidneys/urinary tract. Diagnosis and management \200 Fever/exercise/transient repeat u rine dipstick normal, no treatment \200 Orthostatic age <30yr, no protein in early mornin g, no treatment \200 UTI dysuria, frequency, urine nitrites/leucocytes, culture +ve (b p4 84) \200 Pre-eclampsia pregnancy, iBP oedema (b p504) \200 Myeloma >60yr, bone pain, urine Bence Jones, iCa2+ (b p389) \200 Nephrotic oedema, dalbumin, itriglycerides (b p376 ) DM tight glycaemic and BP control, ACEi (b p330). \200 DM tight glycaemic and BP contro l, ACEi (b p330). Tumor lysis syndrome The destruction of malignant cells during chemothera py causes release of intracellular contents which may overwhelm renal elimination and extra cel- lular buff ers; the resulting metabolic derangement, together with the pre- cipitation of uric acid crystals within the tubules, can cause acute renal failure. Risk factors incl ude pre-existing renal impairment with high-grade tumors, lymphoma or leukemia. Onset is ge nerally within 3d of chemotherapy, with oliguria, muscle cramps, tingling, weakness, tetany and seizures. Blood tests will show iK+, iPO4 3 \210\222, dCa2+, iurate, iurea, icreatinin e. Treatment involves recognition of at-risk patients and prophylactic IV hydration and all opurinol started 24 \200\22348h prior to therapy with careful monitoring of electrolytes du ring therapy. If the syndrome still develops, attempt hyperhydration with IV fl uids, allop urinol, bicarbonate, K+ restric- 3 \210\222 binding under advice from the renal team. Dialy sis may be tion and PO4 necessary to prevent worsening renal failure, refractory hyperkalae mia and ultimately arrhythmias and cardiac arrest. _OHFP.indb 375 _OHFP.indb 375 30/05/2014 16:18 30/05/2014 16:18 376 CHAPTER 12 Fluids and renal Glomerular disease Nomenclature To overcome those palpitations that you experienced as a st udent, remember that the wide range of primary and secondary pathologies aff ecting glomeru li, all share a limited repertoire of clinical manifestations (eg nephrotic syndrome). Thes e pathological processes also share a limited repertoire of histological fea- tures and in the absence of a defi nitive diagnosis, nephrologists will often refer instead to the patte rn seen on biopsy (eg membranous glomerulonephritis). Glomerulonephritis Infl ammation of the glomeruli triggered by an immunologic mechanism res ults in tissue damage, often with proliferation of basement membrane, mesangial cells, or c apillary endothelium. Some important histological types and associated causes and clinical features are listed in Table 12.3. Table 12.3 Classi \201 cation of glomerulonephritis Biopsy Presentation Causes Management Minimal change (normal by light microscopy) Membranous Heavy proteinuria nephrotic syndr ome Nephrotic syndrome (commonest cause in children) ?T cell mediated podocyte damage Majority steroid responsive; very few progress to ESRF 1/3 stabilize with immunosuppression ; 1/3 remit spontaneously; 1/3 progress to ESRF Primary disease may respond to steroids but signifi cant progression to ESRF; secondary disease managed with ACEi Majority self-limiti ng but 20 \200\22340% progress to ESRF; ACEi steroids Idiopathic (70%); malignancy, connective tissue disease, drugs Focal segmental glomerulo - sclerosis Proteinuria nephrotic syndrome; CRF Idiopathic; secondary causes include heroin abuse and HIV Mesangio- proliferative Haematuria (often <72h after URTI); nephritic syndrome Idiopathic IgA deposition Nephrotic syndrome Defi ned as >3g proteinuria/24h with hypoalbuminaemia and oedema. Hyperc holesterolaemia, dIgG and hypercoaguability may also feature. Causes include primary glomer ulonephritis as above (typically minimal change or membranous disease) but also extra-renal causes including DM, anti-GBM disease, malaria, pre-eclampsia and drugs (eg gold, penicill amine, NSAIDs). Treatment is of the underlying cause along with diuretics, active treatment of infection, anticoagulants. Nephritic syndrome Characterized by iBP, oliguria and haematuria. This may classically be s een around 3wk after a streptococcal throat infection as a self-resolving glo- merulonephri tis, but is also associated with some much more aggressive pathologies including vasculitis and anti-GBM disease. OHFP.indb 376 OHFP.indb 376 30/05/2014 16:18 30/05/2014 16:18 377 UROLOGICAL DISORDERS Urological disorders 3Acute urinary retention Causes enlarged prostate, post-operative, pai n, anticholinergics, spinal pathology/MS (painless), pregnancy, constipation, UTI. Symptoms suprapubic pain + urge to urinate, anuria/oliguria, delirium. Signs palpable distended bla dder (dull to percussion and tender), check leg power/refl exes and tone, perianal sensatio n and prostate on PR. Investigations bladder scan if unsure or simply pass a catheter. Mana gement urgent catheterisation (b p546), record residual volume of urine (normal bladder siz e is 400 \200\223500ml, consider acute-on-chronic reten- tion if >1l); urine dipstick and s end for M,C+S; stool chart laxatives; urgent MRI spine if new lower limb neurology and d iminished perianal sensation/ tone (b p357). Beware post-obstructive diuresis: pay close at tention to fl uid balance and electrolytes. Once reversible precipitants addressed, attempt a trial without catheter (TWOC) with close monitoring for recurrence of retention. If this occurs, reinsert catheter and treat as chronic retention. Complications acute renal failur e, chronic obstruction. Chronic urinary retention Causes obstruction (prostate), DM, MS, dy sfunctional bladder. Symptoms incontinence, dribbling, poor stream, recurrent UTI. Signs pa lpable distended bladder (usually non-tender), enlarged prostate. Investigations blds FBC, U+E, PSA, Ca2+, PO4 Management do not catheterise unless in pain or anuric (acute on chroni c retention); refer to urology to investigate cause; options include TURP, intermittent sel f-catheterisation, anti-androgens (eg fi nasteride) or alpha-blockers (eg tamsulosin). Comp lications chronic renal failure, recurrent UTI. Urinary incontinence Types of incontinence: \200 Stress leakage on exercise/coughing/laughing \200 Urge severe and sudden urgency (often due to detrusor instability) \200 Over \202 ow urine volume exceeds bladder capac ity (eg chronic retention) \200 Functional restricted mobility so unable to get to toilet in time. Causes UTI, detrusor instability, neurological problem (eg MS, DM), diuretics + r educed mobility; 5: uterine prolapse, weak pelvic muscles, pelvic mass; 4: post-prostate su rgery. Ask about urgency, frequency, leakage, dysuria, poor stream, haematuria, fl uid inta ke (including caff eine consumption late in the day), eff ects on lifestyle, obstetric hist ory and previous pelvic surgery or trauma, DM, chronic cough, fecal incontinence. If acute presentation with new leg weakness suspect spinal cord compression (b p357). Look for abdo/ pelvic masses, prolapse (b p156); assess leakage on coughing. Investigations urine MSU, glu cose, urinary diary, urodynamics studies. 4: blds PSA (take prior to checking prostate size and nodularity by PR). Treatment general weight loss, less caff eine, stop smoking, treat pro- lapse; stress incontinence fl uid restriction, pelvic fl oor exercises, trans- vaginal tape; detrusor instability behavioral therapy (bladder drill), tolterodine 2mg/12h PO; ove r \202 ow see Chronic urinary retention ; functional aid mobility. 3 \210\222. _OHFP.indb 377 _OHFP.indb 377 30/05/2014 16:18 30/05/2014 16:18 378 CHAPTER 12 Fluids and renal Low urine outputp Worrying features low urine output <0.5ml/kg/h (Table 12.4) sustained >4h or despite adequate fl uid, iHR, systolic BP <100mmHg, iK+, icre- atinine, acidosis. Remember it is easier to treat fl uid overload than acute kidney injury. Table 12.4 Classi \201 cation of low urine output1 Volume in 1h Volume in 24h >60ml (>1ml/kg) <30ml (<0.5ml/kg) <17ml <4ml None >1600ml <800ml <400ml <100ml None Normal urine output Low urine output Oliguria Anuria Absolute anuria 1 Volumes are defi ned for adult patients; in pediatrics values are based upon weight. 3Do not ignore patients with very low urine output, they will be amongst the sickest in the hospital. Think about severe acute kidney injury, shock; most likely hypo- volaemia, hypot ension, urinary retention, blocked catheter, prostatic hypertrophy; other rhabdomyolysis, c hronic renal failure, renal vascular problems (eg thrombosis, emboli), urethral trauma. Ask about abdominal pain, hesitancy, poor stream, fl uid balance (oral and IV intake, vomiting , diarrhea, stoma output, leaking wounds, fever/ sweating), breathlessness, orthopnoea, pos tural dizziness; PMH kidney disease, solitary functioning kidney, prostate disease, iBP, he art disease, DM; DH nephrotoxic drugs (eg NSAIDs, gentamicin, ACEi, IV contrast). Obs BP, H R, RR, fl uid balance, CVP if possible. Look for volume status (b p380), oedema, unrecorded leakage from wounds, stomas or surgical drains; palpable bladder, suprapubic pain, loin pa in, enlarged prostate, evidence of infection or hemorrhage. Investigations urine color, dip stick, M,C+S; septic screen, if not responding to fl uid challenges call for senior help an d send urine for osmo- lality (b p591) and Na+; blds FBC, U+E, CK, osmolality; bladder scan if retention or a blocked catheter is suspected; USS renal tract will allow full assessmen t for structural causes, request a Doppler USS if renal artery stenosis/embolism is suspect ed. Treatment insert a urinary catheter (b p546) and ask the nurses to keep an hourly fl ui d balance including any diarrhea, vomiting and fl uid loss from wounds. Consider asking for a catheter fl ush if already catheter- ised. Assess the patient and if in doubt treat as h ypovolaemia with a fl uid challenge (eg 500ml 0.9% saline over 10 \200\22315min, b p381) an d review in 1 \200\2232h. Beware post-obstructive diuresis if in retention/blocked catheter . If urine output is still low despite treatment then get further senior advice. If a patie nt is volume depleted, it may need considerable fl uid volumes to improve output, but asses s frequently for volume overload. Always rule out urinary tract obstruction. Indiscriminate use of IV furosemide simply to improve output may make the fl uid balance chart look bette r, but does nothing for your patient. OHFP.indb 378 OHFP.indb 378 30/05/2014 16:18 30/05/2014 16:18 379 LOW URINE OUTPUT Table 12.5 Common causes for low urine output History Examination Investigations iurea, concentrated urine, i urine osmolality May have dHb, idWCC, iCRP, i lactate New onset iurea and creatinine, iCK if rhabdomyolysis Persistent iurea and creatini ne, small kidneys on USS Hypovolaemia (b p379) Low fl uid input, excess losses, post-op Negative fl uid balance, iHR, dJVP, dBP (postural) iHR, dBP, iRR, exclude hemorrhage Septic shock (b p480) Malaise, symptoms of infection, acute illness Acute kidney injury (b p372) Severe illness, untreated low urine output May be dehydrated or shocked iBP, lethargy, anorexia, previous kidney problems, DM Chronic renal failure (b p373) Pale, anemic, oedema, bruising, peripheral neuropathy Palpable bladder, often anuric, enlar ged prostate Urinary retention (b p377) Lower abdominal pain, previous prostate problems Full bladder on scan, relief on catheterisation Hypovolaemia This is by far the most common cause of low urine output in in-patients. Sympt oms, signs, investigations see Table 12.5. Treatment increase fl uid input; the rate of reh ydration depends on the patient. If urine output is >0.5ml/kg/h simply increase the rate of current IV fl uids. If <0.5ml/kg/h consider a fl uid challenge (b p381) and prescribe some quick fl uids to follow, eg 0.9% saline 1l/4h; review the patient in 1 \200\2232h. Complic ations acute renal failure. Fluid overload Prescribing of fl uid volumes that exceed the ability of the kidneys to excr ete may lead to iatrogenic fl uid overload (eg failure to identify obstructive uropathy or cardiac failure as cause of low output). Symptoms, signs, investigations (see b p380). Trea tment (see b p282 \200\230Pulmonary oedema \200\231). For mild overload reduce or stop IV fl uids and review in a few hours; ask the nurses to record hourly obs and contact you if t he patient \200\231s RR rises. If you are certain of overload, ensure no evidence of obstru ction before trying 40mg furosemide IV. This will cause a diuresis in most patients, but po tentially contribute towards acute renal failure if the patient was hypovolaemic. In certai n settings (eg sepsis + cardiogenic shock) the patient may be intravascularly volume deplet ed, but symptomatically fl uid overloaded \200\223 this requires senior assess- ment for H DU/ICU and inotropic support. Complications pulmonary oedema. y Causes of low urine output covered elsewhere b p473 Cardiac failure b p267 Hypotension/shock _OHFP.indb 379 _OHFP.indb 379 30/05/2014 16:18 30/05/2014 16:18 380 CHAPTER 12 Fluids and renal IV \202 uids 1 Assessing volume status HR, postural hypotension and low urine output (<0. 5ml/kg/h) are sensitive signs of hypovolaemia while orthopnoea suggests overload. Table 12.6 Assessing volume status History durine output, headache, thirst or poor oral intake, excessive fl uid loss (eg diar rhea, vomiting) Drowsy, obtunded Oliguria/anuria, dBP<100mmHg, sunken eyes, decreased skin turgor iRR, dO2 sats, iJVP, bilateral basal crackles, pitting oedema,3 gallop rhythm (3rd h eart sound) Examination iHR,1 postural BP drop,2 urine output <0.5ml/kg/h, dry mucous membranes, capill ary refi ll >2s, dJVP Investigations Dark urine, iurine osmolality; blds: iurea, iPCV/ haematocrit, ialbumin, ise rum osmolality icreatinine Mild- moderate fl uid defi cit (eg <1500ml in adult) Severe hypovolaemia (as for mild plus \200 ) Fluid overload Cardiac history, Pulmonary oedema on CXR (b p582), abnormal ECG (b p572 \200\223 LVH, MI), iCVP excess fl uids, SOB, orthopnoea, cough, sputum (white/ frothy), swelling 1 Including upper range of normal, ie >90/min; remains slow if taking B-blockers or other rate limiting drugs (eg verapamil, diltiazem, digoxin). 2 A drop of >20mmHg systolic/10mmHg diastolic is signifi cant. 3 Ankles if sitting, sacrum if in bed. Fluid balance is calculated by measuring a patient \200\231s urine output and fl uid input along with any losses from vomit, diarrhea, or drains. The patient must be catheterised for accurate measurement. Insensible losses are unrecordable fl uid losses, eg sweating and breathing. 500 \200\22310 00ml is usually lost each day, but this increases with pyrexia (from sweating), tachypnoea and burns; this loss will not be apparent from the fl uid chart. Litres of fl uid can be lo st from burns and wound seepage which is missed unless the bandages are inspected. Third-space \202 uids Also called \200\230fl uid sequestration \200\231; infl ammation a nd injury causes capillary permeability to increase so that fl uid and protein leak from th e blood vessels (intravascular space) causing oedema. The patient is intravascularly hypovo laemic despite normal fl uid balance and fl uid should be replaced according to clinical si gns, especially urine output. It is common in sepsis, pancreatitis and after major operatio ns. CVP lines Central venous pressure measurements are used primarily in ICU and HDU since they require a central line (b p534). By recording the pressure in the line at the level of the right atrium, an estimate of fi lling state is obtained. The normal range is 1 \200 \2237mmHg (1 \200\2239cmH2O); high pressure suggests fl uid overload or heart failure while a low CVP suggests hypovolaemia. Trends are more important than absolute values; the CVP s hould rise with a fl uid challenge; hypovolaemia has been corrected once this rise persists after the challenge has fi nished, or when there is no further rise in CVP with subsequent fl uid challenges. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG174 OHFP.indb 380 OHFP.indb 380 30/05/2014 16:18 30/05/2014 16:18 381 IV FLUIDS 3Resuscitation \202 uids Rapid restoration of circulating volume is vital, particularly f or those with evidence of severe hypovolaemia (Table 12.6). Give high-fl ow O2, estab- lish IV access and begin emergency management (b p472). Fluid challenge This implies rapid deli very of a bolus of fl uid with monitoring for eff ects to guide further fl uid management. A bolus of 500ml crystalloid eg 0.9% saline IV (250ml if frail or heart problems, 10ml/kg i n children) is infused over <15min. Reassess immediately: If evidence of hypovolaemia persi sts, consider further 250 \200\223500ml fl uid boluses. Large volumes may eventually be nee ded, but seek senior help and involve ICU early. eventually be needed, but seek senior help and involve ICU early. Choice of \202 uid in resuscitation Choice of synthetic resuscitation fl uid has historically split into a debate between the u se of crystalloids (aqueous solutions of mineral salts) and col- loids (containing larger, insoluble molecules). Although colloids might theo- retically exert an osmotic load keeping more fl uid in the circulation, this eff ect may be overstated and must be set against the higher cost of colloids. Recent trial data have fi rmly come down in favor of the use of c rystalloids, with evi- dence of increased rates of renal failure1 and death2 associated wit h colloid resuscitation. Evidence for choice of crystalloid is less robust, and both 0.9% s aline and physiological salt solutions represent reasonable choices. Of course, blood repre sents a highly physiological replacement fl uid when used in hemorrhage, but is rarely a pr actical or necessary choice in other settings. Human albumin solutions should off er the sa me osmotic bene- fi ts as proposed for colloids, but in ICU study data any survival advanta ge appears small and limited to patients with severe sepsis.3 1 Myburgh, J.A. et al. NEJM 2 012 367:1901 available free at (cid:27)www.nejm.org/doi/ full/10.1056/NEJMoa1209759 2 Perner, A. et al. NEJM 2012 367:124 available free at (cid:27)www.nejm.org/doi/full/10.10 56/ NEJMoa1204242 3 SAFE study investigators NEJM 2004 350:2247 available free at (cid:27)www.nejm.org/doi/ full/10.1056/NEJMoa040232 Maintenance \202 uids Prescribing routine fl uids is a common task for foundation docto rs, and one your seniors are unlikely to take much interest in until you make a mistake. Wh en asked to prescribe fl uids, always consider why a patient is on fl uids, what their elec trolyte needs are (look at recent blood result), and whether further fl uids should be give n (is the patient able to drink?) If in any doubt, assess the patient for RR, JVP, and basa l lung creptitations. Maintenance requirements Typically adults require 25 \200\22330ml of water/ kg/24h to cover their urine output and insensible losses (sweat, respi- ration, stoo l). This equals about 2 \200\2232.5l per day for a 70 \200\22380kg adult.1 Several addition al sources of fl uid losses may occur in acutely ill patients: \200 Recordable polyuria, NG aspirate, diarrhea, vomiting, drains \200 Insensible wound leakage, pyrexia, tachypnoe a, burns \200 Third space (b p380), eg pancreatitis, post-op. As much as possible, intake should come through the GI tract \200\223 always maximize PO intake, and consider using N G fl uids as an alternative to IV where inadequate PO intake persists \211 3d. Alternative ly, for an elderly patient managing insuffi cient volumes PO and who has no need for an IV cannula, 1l 0.9% saline SC overnight (12h) may be all that is required. Always explore with seniors which patients need to remain NBM. 1 Pediatric fl uid requirements are on b p383. _OHFP.indb 381 _OHFP.indb 381 30/05/2014 16:18 30/05/2014 16:18 382 CHAPTER 12 Fluids and renal Estimating \202 uid requirements 24h requirements can best be estimated from review of an accurate fl uid balance chart. This is especially useful in patients at risk of fl uid ove rload. Three components need to be considered: \200 Recorded losses over last 24h (from f l uid chart) \200 Estimate of insensible losses (usually 0.5 \200\2231.5l/24h) \200 Est imate of fl uid defi cit (from history, examination, obs and fl uid chart). Where a fl uid balance chart is not available, estimate needs as: \200 Estimate of maintenance requireme nt from weight (25-30ml/kg/24h) \200 Additional fl uids if signifi cant insensible losses are expected (0.5 \200\2231.5l/24h) \200 Estimate of fl uid defi cit (from history, exam ination, obs). Beware groups of patients who may need less fl uids than estimated: elderly/ frail, low BMI, heart problems, renal failure, partial oral intake. Electrolyte and glucose requirements Estimation of electrolyte requirements should take into account current U+E, medications (especially diuretics and supplements) and fl uid loss. Basic maintenance requi rements are: \200 Na+, K+, Cl- 1mmol/kg/24h \200\223 eg typically 60 \200\22380mmol a da y \200 Glucose 50 \200\223100g/24h \200\223 5% glucose contains 5g/100ml. Table 12.7 sho ws the electrolyte content of some commonly used IV fl uids. Due to potential to trigger dy srhythmias, the maximal safe rate of potassium administration outside of HDU/ICU is 10mmol/ h. Table 12.7 Electrolyte constituents of common IV \202 uids Na+ (mmol/l) K+ (mmol/l) Cl \210\222 (mmol/l) 5% glucose Glucose saline1 0.9% saline2 Hartmann \200\231s Packed red cells: Fresh At expir y date 0 30 154 131 0/20/40 0/20/40 0/20/40 5 0 30 154 111 15 10 0.3 6.0 150 150 1 0.18% saline/4% glucose. 2 1l 0.9% saline/24h already exceeds daily Na+ requirements. Lar ge volume saline infusions result in hyperchloraemic metabolic acidosis and potential overl oad of renal sodium excretion capacity. Prescribing Having decided the 24h fl uid and electrolyte requirement, convert total needs into suitable 500 \200\2231000ml bags to run at appropriate rates. If there is any defi cit the initial bags should be run more quickly to correct hypovolaemia. Where safe, prescribe the fl uids so that they run out during the normal working day to reduce work for those on -call; if careful review is required before further fl uid prescribing, this should be indi cated on the chart. A maintenance fl uid regimen suitable for an otherwise well hospitalize d patient who is NBM awaiting surgery is shown in Fig. 12.1. Although this may be appropria te for an adult with a healthy heart and kidneys, indis- criminate use of this regimen coul d lead to fl uid overload. Signature Date 19.8.14 19.8.14 19.8.14 Route Fluid IV IV IV Additives 40mmol KCl Vol 1l 500ml 1l Rate 10h 4h 10h 5% glucose 0.9% saline Nil 5% glucose ALJRivett ALJRivett ALJRivett 20mmol KCl Fig. 12.1 Example of a maintenance fl uids regimen. OHFP.indb 382 OHFP.indb 382 30/05/2014 16:18 30/05/2014 16:18 383 IV FLUIDS Special cases Post-op Patients may leave surgery with hypovolaemia due to blood loss and th ird space loss; they may require more fl uids to make up this defi cit. Despite lysis of ce lls during surgery causing a release of K+, most post- operative patients who remain NBM wi ll still require supplementary KCl in their post-operative fl uid replacement after 24h. Intestinal \202 uid losses Most intestinal fl uids have a composition similar to 0.9% sal ine with 20mmol/l of KCl and should be replaced with this. For the exact composition of dif f erent intestinal fl uids see section 9.2 of the BNF. Heart problems Patients with previou s heart disease are more prone to fl uid overload and pulmonary oedema. Simple attention to fl uid balance prevents problems in the majority of patients. If fl uid overload develops the patient may require a dNa+ diet, daily weights and fl uid restriction (eg 1.5l/24h). Th ere is no logic to the routine prescribing of furosemide alongside maintenance fl uids. Chr onic liver failure Excess Na+ may cause ascites. Restrict Na+ by using 5% glucose; 1.5l/24h fl uid restriction is sometimes required. If fl uid resuscita- tion is required use salt-p oor albumin (a blood product, see BNF section 9.2.2.2). Recheck U+E regularly to ensure not becoming hyponatraemic. Acute renal failure Ensure adequate and timely administration of crys- talloids to correct for any hypovolaemia. Avoid additional K+ unless hypokalaemic. Further IV fl uids should be determined by fl uid balance CVP in HDU/ICU, along with regular repeat U+E. Chronic renal failure A reduction in glomerular fi ltration rate (GFR) means that the kidne y cannot excrete as much water, Na+ or K+. In mild renal failure excess fl uids and Na+ sho uld be avoided, though acute deteriora- tion in renal function is usually a sign of hypovol aemia. In severe renal failure restriction of Na+, K+ and fl uid (eg 1.5l/24h) is required. 3If in doubt Reassess and seek senior advice. Fluid prescribing is complex, the condition of your patient will change and there is no substi- tute for reassessing prior to prescribi ng the next bag of any fl uid. Children \200\231s maintenance \202 uids1 Milk volume babi es >5d require 150ml/kg milk each day. Maintenance calculate daily fl uid (oral/IV) require ments from Table 12.8. Table 12.8 Maintenance \202 uids in children Weight fi rst 10kg 10 \200\22320kg above 20k g Fluids/kg/24h 100ml/kg/24h 50ml/kg/24h 20ml/kg/24h Fluids/kg/h 4ml/kg/h 2ml/kg/h 1ml/kg/h Expected 24h volume 0 \200\2231000ml 1000 \200\2231500ml 1500 \200\2233000ml Example 23kg child: (10 x 100ml) + (10 x 50ml) + (3 x 20ml) = 1560ml/24h. 1 Children are especially prone to iatrogenic electrolyte disturbances, especially hypo- an d hypernatraemia, both of which can be fatal. Therefore, fl uid choice requires specialist ad vice; 5% glucose + 0.45% saline is safe in most situations. _OHFP.indb 383 _OHFP.indb 383 30/05/2014 16:18 30/05/2014 16:18 384 CHAPTER 12 Fluids and renal Potassium emergencies Check airway is patent; consider maneuvers/adjuncts If no respiratory eff ort \200\223 CAL L ARREST TEAM If no palpable pulse \200\223 CALL ARREST TEAM Airway Breathing Circulation 3Call for senior help early if patient deteriorating. Hypokalaemia (K+<2.5mmol/l or <3mmol/ l with ECG changes) \200 ECG changes: arrhythmias, prolonged PR interval, ST depression, small/inverted T waves, U waves (after T wave) 15l/min O2 if SOB or sats <94% \200 Monitor defi brillator \200\231s ECG leads, BP, pulse oximeter \200 Venous access, take bloods for urgent repeat U+E, Mg2+ \200 Replace K+, 40mmol/l KCl in 1l 0.9% saline IV unless oliguric do not replace K+ faster than 10mmol/h outside of HDU/ICU \200 never give KCl STAT ABG to exclude severe alkalosis \200 Call for senior help \200 Reassess, starting with A, B, C \200 Hyperkalaemia (K+ \211 7mmol/l or >5.3mmol/l with ECG changes) \200 ECG c hanges: arrhythmias, fl at P waves, wide QRS, tall/tented T waves 15l/min O2 in all patients \200 Monitor defi brillator \200\231s ECG leads, BP, pulse oxi meter \200 Venous access, take bloods for urgent repeat U+E \200 If ECG changes seen or K+ \211 7mmol/l (arrhythmias, b p248): 10ml of 10% calcium gluconate IV over 2min, repeat every 15min up to 50ml (fi ve doses) until K+ corrected 10 units Actrapid in 50ml of 50% glucose over 10min \200 salbutamol 5mg nebuliser \200 ABG to exclude severe acidosis \200 Consider Calcium Resonium 15g PO or 30g PR \200 Call for senior help \200 Reassess, starting with A, B, C \200 Life-threatening causes Hyperkalaemia \200 Renal failure \200 Acidosis \200 Tissue necrosis Hypokalaemia \200 Hypovolaemia \200 Alkalosis OHFP.indb 384 OHFP.indb 384 30/05/2014 16:18 30/05/2014 16:18 385 ELECTROLYTE IMBALANCE Electrolyte imbalance 3Hypokalaemia (K+<3.5mmol/l) Worrying features dGCS, chest pain, palpitations, abnormal ECG. Causes vomiting, diarrhea, most diuretics, steroids and Cushing \200\231s, inad- equate rep lacement in fl uids, alkalosis, Conn \200\231s syndrome. Symptoms weakness, cramps, palpitations, nausea, paraesthesia. Signs muscle weakness, hypotonia, arrhythmias. Investigations blds recheck U+E looking for coexisting electrolyte imbalances, in particula r dMg2+ ABG if alkalosis suspected ECG T wave fl attening or inversion, U waves, ST depress ion, atrial arrhythmias. Treatment if K+ \211 2.5mmol/l with no ECG changes add 20 \200 \22340mmol KCl to IV fl uids or give Sando-K 2 tablets/8h PO and monitor U+E; con- sider writing up Sando-K only for 3 \200\2235d to prevent continuous unmoni- tored treatment. R eplace any concurrent dMg2+ (eg 8mmol MgSO4 in 100ml 0.9% saline IV over 1h). If K+ <2.5mmo l/l or ECG changes see treatment plan, b p384. 3Hyperkalaemia (K+ >5.3mmol/l) Worrying features dGCS, chest pain, palpitations, abnormal ECG. Causes haemolysed samples (likely if several hours taken to reach lab), renal failure, K+-s paring diuretics (spironolactone, amiloride), ACEi, trauma, burns, excess K+, large blood t ransfusions, Addison \200\231s disease. Symptoms palpitations, dizziness, chest pain. Signs assess haemodynamic stability, irregular pulse, stigmata of renal failure. Investigat ions blds urgent repeat U+E; if K+<7mmol/l with no new ECG changes or the sample is reporte d as haemolysed then await the repeat sample, otherwise follow the treatment plan (b p384); if on digoxin, check levels since digoxin toxicity will worsen hyperkalaemia; ABG for acid osis if acute renal failure ECG initially peaked T waves, later broad QRS and fl at P waves , ultimately VF. Treatment Ca2+ gluconate protects the heart against iK+. Salbutamol and in sulin move K+ into cells to reduce plasma levels in the short term (1 \200\2232h) after whi ch a rebound increase may occur. Furosemide (with IV fl uids if necessary) or Calcium Reson ium (takes 24h, give with lactulose 30ml/6h PO) enhance K+ excretion. If refractory or ac idotic, dialysis may be neces- sary (b p373). Stop any causative or nephrotoxic medication. _OHFP.indb 385 _OHFP.indb 385 30/05/2014 16:18 30/05/2014 16:18 386 CHAPTER 12 Fluids and renal Hyponatraemia (Na+ <133mmol/l) Worrying features dGCS, irritable, seizures, iHR, dBP. Ask about diarrhea, vomiting, abdo pain, tiredness, urine frequency, quan- tity and color, thirst, constipation, SOB, cough, chest pain, weakness, head trauma; PMH heart, liver or ki dney problems; DH diuretics, opioids, antipsychotics, amiodarone, proton pump inhibitors, S SRIs, IV fl uids. Look for assess fl uid balance and volume status (b p380), basal creps, o edema (legs and sacrum), ascites, focal neurology, conscious level (if Na+ <120mmol/l the p atient may become irritable or confused, <110mmol/l there may be seizures or coma). Investi gations blds FBC, U+E, LFT, CRP, plasma osmolality; urine send paired sample for osmolality and Na+; assess underlying cause as follows: Hypovolaemic? p380 Yes No Urine Na+ >20mmol/l? Oedema? Yes No No Yes Hypovolaemia due to renal losses, eg diuretics, Addison \200\231s, salt-losing nephropathy Hypovolaemia due to non-renal losses eg diarrhea, vomiting, fistulae, burns, small bowel ob struction, heat exposure Consider excess 5% glucose or oral fluids, severe hypothyroidism, or SIADH (see box) Consider heart failure, renal failure and nephrotic syndrome, liver failure Fig. 12.2 Assessment of hyponatraemia. Spurious dNa+ (pseudohyponatraemia) can be caused by taking blood from an arm with IV fl uids running, a lipaemic sample (labs should detect th is) or osmotically active substances in the blood, eg in hyperglycaemia. Discuss with lab i f unsure. Syndrome of inappropriate ADH secretion (SIADH) In this condition, inappropriate hypothalam ic release of ADH leads to euvolaemic hyponatraemia. Beware of overcalling this diagnosis, which requires a careful workup: \200 Concentrated urine despite dilute plasma (ie urine osmolality > plasma): generally plasma osmolality <275mosm/kg and urine osmolality >500mosm/kg No recent diuretics \200 Clinical euvolaemia \200 Urine sodium >20mmol/l Causes include malignancy (lung, pancreas, lymphoma), lung infec- tions, CNS infections or vascular event s, drugs (eg SSRIs, tricyclics, carbamazepmine, antipsychotics) or idiopathic. Management r equires fl uid restriction (initially 1l/24h) ADH antagonists (eg demeclocy- cline 300mg /12h PO). Normal adrenal and thyroid function (check TSH and short Synacthen test). OHFP.indb 386 OHFP.indb 386 30/05/2014 16:18 30/05/2014 16:18 387 ELECTROLYTE IMBALANCE Treatment Although acute hyponatraemia (<48h duration) can be rapidly corrected, chronic hy ponatraemia (or where the timecourse is unclear) should be corrected slowly to prevent fl u id overload or osmotic demyelination. Aim for a rise of no more than 10mmol/l/24h. Get seni or help if seizures or coma (the rare situation where it may be necessary to raise Na+ rapi dly by 75mmol/l using hypertonic saline) or if Na+<120mmol/l. In all patients monitor fl ui d balance closely with cath- eter, regular obs and possibly CVP. Repeat U+E daily, or more frequently if neurological signs. Assess cause using Fig. 12.2 and treat accordingly. \200 Hypovolaemic replace lost fl uid with 0.9% saline according to degree of dehydration (b p 382); severe hypovolaemia should be corrected (b p478) and takes precedence over hyponatrae mia. Try to establish the cause of fl uid loss and treat accordingly. Stop diuretics \200 Normovolaemic or mild overload slow 0.9% saline IV eg 1l/8 \200\22310h, Na+ levels should rise over a few days. If urine osmolality >500mOsmol/kg consider SIADH (see box) Oedematous urine Na+ usually <10mmol/l, identify and treat the underlying cause (see relevant chapter). Causes of hyponatraemia covered elsewhere b p373 b p376 b p267 b p313 Heart failure Liver failure Renal failure Nephrotic syndrome Hypernatraemia (Na+ >146mmol/l) Worrying features dGCS, iHR, dBP. Causes fl uid loss (diarrhea, burns, fever, glycosuria eg DM, diabetes insip- idus) or inad equate intake (impaired thirst response in elderly or hypo- thalamic disease); more rarely excess Na+ (iatrogenic, Conn \200\231s syndrome). Symptoms anorexia, nausea, weakness, hype rrefl exia, confusion, dGCS. Signs assess fl uid balance, volume status (b p380), neurologi cal defi cit. Investigations blds plasma osmolality (likely to be raised); urine osmolality (>400mOsmol/kg if fl uid loss, <400mOsmol/kg if excess Na+, normal range 350 \200\2231000m Osmol/kg); consider CT head or MRI if suspect central cause. Treatment cells rapidly adapt to raised osmolality of extracellular fl uid by retention and production of intracellular osmolytes. This prevents osmotic fl uid losses from inside the cell, but if extracellular Na+ concentration rapidly corrected, osmotic forces will now dr ive fl uid into cells, causing lysis resulting in neurological damage and death. Hence aim for slow correction of Na+ (10mmol/l/24h at the very most). Treatment is guided by volume s tatus: \200 Hypovolaemic give 0.9% saline 1l/6h (prevents sudden Na+ shifts) until normovolaemic Normovolaemic encourage oral fl uids or 5% glucose 1l/6h. Monitor fl uid balance and plasma Na+; consider a urinary catheter. _OHFP.indb 387 _OHFP.indb 387 30/05/2014 16:18 30/05/2014 16:18 388 CHAPTER 12 Fluids and renal Hypocalcaemia (corrected Ca2+<2.2mmol/l) Although >99% calcium is stored in bones, and most of the remainder is intracellular, extracellular calcium is critical for neuromuscular and cardiac function. Albumin binds around 40% of extracellular calcium, so hypoalbuminaemia m ay give falsely low recordings of serum calcium; always check the \200\230corrected calciu m \200\231. Gut, renal, and bone calcium han- dling is critically regulated by vitamin D, w hich requires hydroxylation in functioning kidneys and liver to be active, and by PTH. Worrying features dGCS, chest pain, palpitations, dBP, abnormal ECG. Causes vitamin D defi ciency (elderly, Asians, Africans, chronic renal failure, intestinal malabsoprtion eg coeliac, Crohn \200\231s), hypoparathyroid, acute pancreatitis, alkalosis, dMg2+, alcoholism. Symptoms spasm of hands and feet (carpopedal), twitching muscles, tingling around the mouth , fatigue, depression, dry skin, coarse hair.