vestibular features. p y Key questions in \200\230dizziness \200\231 The sensation of dizziness is diffi cult to de scribe ( \200\230giddy \200\231, \200\230funny do \200\231, \200\230muzzy headed \200\231 ) and refl ects some critically diff erent underlying pathologies; try to map your patient \200\231s symptoms onto a medical equivalent by asking about: \200 Loss of consciousness suggests seizures (b p346) or syncope (b p260). The impending sense of loss of consciousnes s, often with a \200\230graying out \200\231 of vision, is described as presyncope; causes and management are similar to syncope Postural symptoms are worse on standing after a sedentary period; this suggests postural hy potension and should prompt a review of medications Vertigo is the sensation of the world moving or spinning about the patient and is worse on sudden head movements; this suggests a problem with the labyrinth, vestibular nerve or brai nstem (b p363) \200 Ataxia is shown by the inability to stand or walk straight; patients may have problems with fi ne limb movements; this suggests problems with proprioception or cerebellar function (b p363). Always ask about onset, deterioration, hearing loss, tinnitus, nausea, vomiting. Romberg \200\231s test1 The cerebellum normally receives information needed to keep us upri ght from 2 sensory systems: vision and proprioception (via the spinal dorsal columns). Norm ally, one system can compensate for loss of the other. With the eyes closed and the feet pl aced together, a patient who sways exces- sively or falls is \200\230Romberg +ve \200\231, having lost proprioception. With a cerebellar lesion, the patient will struggle to maintai n posture even with the eyes open. 1 Described by the pioneering C19th German neurologist M oritz Romberg, working amongst the destitute of Berlin with tabes dorsalis (tertiary neurosyphilis). OHFP.indb 362 OHFP.indb 362 30/05/2014 16:18 30/05/2014 16:18 363 DIZZINESS Vertigo (OHCS8 b p554) ) g ( p Worrying features focal neurology, multidirectional or non-fatiguing nystagmus. Treat the sensation of vertigo whilst determining the underlying cause. Centrally acting an tihistamines (eg cyclizine 50mg/8h PO) and pheno- thiazines (eg prochlorperazine 5mg/8h PO) are particularly eff ective; betahistine 16mg/8h PO may also be used. Benign positional ve rtigo Sudden onset vertigo lasting seconds following specifi c head movements. Treated with Epley maneuver (a series of movements to dislodge the vestibular debris causing the sympto ms OHCS8 b p555) and referral to physiotherapy for vestibular exercises. Inner ear in \202 ammation causes sudden onset vertigo, nystagmus and severe nausea without focal neurology. Reassure and treat as above. \200 Vestibular neuronitis viral infection of the vestibula r nerve; improves within 1 \200\2232wk but can take 2 \200\2233mth to fully resolve Labyrinthitis as for vestibular neuronitis with hearing loss or tinnitus. M ni re \200 \231s attacks of severe vertigo lasting several hours, with tinnitus and progressive low fr equency hearing loss. Treat as above, and refer to ENT. Motion sickness rarely encountered in hospital, however cinnarizine j 30mg PO 2h before journey is eff ective. g y Nystagmus is found with many peripheral and central causes of vertigo. Causes include: stro ke, MS, space occupying lesions, labyrinthitis, ves- tibular neuronitis, benign positional vertigo, trauma, drugs of abuse (alcohol, LSD, PCP, ketamine), medications (lithium, SSRIs, phenytoin), M ni re \200\231s, Wernicke \200\231s encephalopathy; congenital (rare). Imbalance/ataxia Ataxia can be diff erentiated from vertigo on history; there are two types : \200 Cerebellar \200\230DANISH \200\231 signs (see earlier in this topic); unstable ev en with eyes open Sensory Romberg \200\231s +ve (see box), loss of proprioception, preservation of fi ne coordination; \200\230stamping \200\231 gait, spinal/neuropathy signs. Cerebellar ataxia Causes CVA, multiple sclerosis, alcohol toxicity, Wernicke \200\231s ence ph- alopathy, phenytoin, B12 defi ciency, normal pressure hydrocephalus, infection, space-o ccupying lesions, trauma, paraneoplastic. Management MRI is the most useful diagnostic test (consider CT if acute onset), neurology referral, some underlying causes are treatable: \200 Wernicke \200\231s encephalopathy thiamine (B1) defi ciency often as a result of chro nic alcohol excess results in confusion, ataxia, ophthalmoplegia, and nystagmus; treated wi th thiamine (PO/IV, b p218), as for Korsakoff \200\231s syndrome, to which it may progress if left untreated. Sensory ataxia Causes cervical spondylosis, MS, peripheral neuropathy, syringomyelia, spina l tumor, spinal infection, B12 defi ciency, Friedreich \200\231s ataxia, syphilis. Manageme nt urgent MRI if acute onset, otherwise consider tests for peripheral neuropathy (b p355), spinal X-rays, routine MRI, nerve con- duction studies, neurology referral; often treated w ith B12. _OHFP.indb 363 _OHFP.indb 363 30/05/2014 16:18 30/05/2014 16:18 364 CHAPTER 11 Neurology and psychiatry Aggressive behavior emergency Stay between the aggressor and the exit \200 Get extra help from other staff and/or secur ity \200 Consider phoning the police. Safety 3Call for senior help/security early if the situation is deteriorating. \200 Assess the s afety is anyone at acute risk? \200 Emergency sedation if they are a risk to themselves o r others1 \200 lorazepam 1 \200\2232mg (1mg elderly/renal failure) PO/IM/IV STAT \200 h aloperidol 5 \200\22310mg (2mg elderly) PO/IM/IV STAT \200 Can be used together or separa tely Try to establish the precipitant from staff /relatives \200 Ask a member of staff who kno ws the patient to accompany you \200 Invite the patient to sit down with you and discuss the problem \200 Listen until they feel they have explained the problem \200 Assess the patient for signs of psychosis or acute confusion \200\223 are they physiologically unwell, psychologically disturbed or merely angry Apologize and/or off er sympathy as appropriate \200 Address any concerns raised by the p atient \200 Ask specifi cally about pain or worry \200 Consider off ering oral sedation or analgesia \200 Attempt to defuse the situation \200 If unsuccessful contact a senio r for help.p Common causes Acute confusion (delirium) b p341 \200 Intoxication (drugs/alcohol) \200 Psychosis due to an underlying psychiatric disorder b p365 \200 Anger/frustration/poor communication b p21 \200 Pain b p86 \200 Hypoxia b p270 \200 Hypoglycaemia b p323. Sectioning and the Mental Health Act 2007 In England and Wales, this Act allows the hospitalization of individuals who are believed t o be aff ected by a mental illness that: \200 Requires assessment or treatment and \200 Is suffi ciently serious to pose a threat to self or others and \200 Requires hospitaliz ation to which they are unable/unwilling to consent. If you feel this applies to your patie nt, speak to your seniors and the psy- chiatrist on call urgently. Critically, these powers only apply to detention for the purposes of assessment or treatment of mental illness and cannot be used to detain for treatment of physical illness. In this case, treatment deci- s ions should be based upon an assessment of mental capacity (b p28). In Scotland and Norther n Ireland, similar powers are granted under the Mental Health Act 2003 and Mental Health Or der 1986 respectively. 1 If a patient poses a risk to themselves or others any doctor can give emergency sedation, without the patient \200\231s consent and with restraint, under the Mental Capacity Act (2 005). OHFP.indb 364 OHFP.indb 364 30/05/2014 16:18 30/05/2014 16:18 365 MOOD DISTURBANCE/PSYCHOSIS Mood disturbance/psychosis Worrying features delusions, hallucinations, suicidal intent. p y Think about emergency acutely suicidal; psychosis schizophrenia, depression, bipolar disord er, postpartum, substance abuse, alcoholism or withdrawal; low mood depression, bipolar dis order, anxiety disorder, per- sonality disorder, eating disorder, seasonal aff ective disor der, postpartum, grief, alcoholism or withdrawal, substance abuse; high mood bipolar dis- o rder, cyclothymia, substance abuse; organic endocrine (hypo/hyperthy- roid, Cushing \200 \231s, Addison \200\231s), neurological (CVA, dementia, MS, Parkinson \200\231s, head injur y, brain tumor), infections (HIV, Lyme disease, EBV syphilis), imbalance infl ammatory dise ase (eg rheumatoid, SLE), electrolyte (eg Na+, Ca2+), metabolic problems (eg porphyria, Wil son \200\231s), malnutri- tion, anemia, paraneoplastic, medications (b p366). See Table 11. 11. Ask about (see psychiatric history b p160) medical bowel habit, weight change, appetite , cold/heat intolerance, tremor, previous head trauma, changes in vision, headaches, unusua l sensations, weakness, sei- zures, sleeping problems, sexually transmitted illnesses and r isk, rashes, joint pain; psychiatric early morning waking, concentration, energy levels, la ck of pleasure, appetite, recent stresses, mood, change in personality, suicidal ideation; personal childhood, education, employment, relation- ships; forensic previous criminal conv ictions, custodial sentences; PMH previous psychiatric problems or care, mania, suicide att empts, chronic illness; DH regular medications, alternative medicines; FH psychiatric probl ems, thyroid, liver or brain problems, occupations; SH who do they live with, family, frien ds, alcohol intake, smoking, illicit substance abuse. Obs GCS, temp, HR, BP, RR, glucose. L ook for (see mental state examination b p160) medical full systems exam and careful neurolo gical exam including tremor, eye refl exes, pap- illoedema, tendon refl exes; psychiatric g eneral appearance, signs of neglect or fl amboyancy, unusual posture or movements, aggressi on, aff ect, speech (form and content), thought (form and content including delusions), per ception including hallucinations, cognition (concentration, memory, orientation), risk (to self or others), insight. Investigations it is important to consider organic causes of ment al disturbance. blds consider: FBC, U+E, LFT, Ca2+, TFT, ESR, ANA, B12, folate, cortisol, H IV (b p490), EBV and Lyme disease serology, VDRL/ THPA; urine toxicology screen; LP, EEG, C T/MRI brain. Management \200 Is the patient manic, psychotic (delusions or hallucinations, b p162) or acutely suicidal? If so they need urgent psychiatric referral Could there be an organic cause for their symptoms (see earlier in topic)? \200 Is the pa tient already known to local community mental health team? \200 For milder symptoms would their GP or the local crisis team be better placed to manage in community? _OHFP.indb 365 _OHFP.indb 365 30/05/2014 16:18 30/05/2014 16:18 366 CHAPTER 11 Neurology and psychiatry Table 11.11 Common causes of mood disturbance and psychosis History Examination Investigations Low mood, tearful, loss of interests, sleep disturbance Poor eye contact, neglect, low mood and aff ect, psychosis Signs of high or low mood, p sychosis Neglect, poverty of speech/thought Fearful, tense or normal Evidence of self- harm , usually normal Neglect, poor cognition with normal consciousness Neurological signs, rash es, wasting Usually normal Depression Mixture of low and high mood events Usually normal Bipolar disorder Schizophrenia Delusions, auditory hallucinations, apathy Worry, sweating, dizziness, palpitations Longstanding diffi culties Problems with memory, concentration, cog nition Usually normal Usually normal Anxiety Usually normal Personality disorder Dementia May have abnormal CT/ MRI brain Organic cause Weight loss, seizures, Usually abnormal rapid onset, visual hallucinations Bipolar disorder Recurrent episodes of high mood, usually interspersed with episodes of low mood. High mood may be mania (impairs job or social life and may have psychotic features) or hypomania (no impairment to job or social life). DSM-51 classifi es bipolar disorder as occurring after even a single episode of mania; ICD-101 classifi es this as a manic episode , and reserves \200\230bipolar disorder \200\231 to describe recurrent episodes of mania, or mania with depressive episodes. Recurrent swings between mild depression and hypomania a re called \200\230cyclothymia \200\231. Mania signs fl amboyant dress/appearance, excess/r apid speech, easy distractibility, restless. Investigations if fi rst manic episode: CT hea d; EEG; urine toxicology. Treatment consider admission based on severity of episode and ris k to self (suicide or reputation), job, assets, relationships. Mania is treated acutely wit h antipsychotics (particularly olanzapine) and benzodiazepines. Antidepressants are used fo r depressive episodes but may precipitate mania. Preventive treat- ment is with lithium, ca rbamazepine, valproate, or lamotrigine. Complications fi nancial errors, criminal activity, unemployment, relationship breakdown, suicide. Examples of medications with psychiatric side eff ects NSAIDs, antihypertensives, B-blocker s, digoxin, oral contraceptive pill, antiepileptics, corticosteroids, antibiotics, cytotoxi cs, levodopa, anticholinergics, sedatives These may all aff ect mood, cognition or exacerba te underlying psychiatric disease 1 See box b p161 for details of the DSM-5 and ICD-10 classifi cation systems. OHFP.indb 366 OHFP.indb 366 30/05/2014 16:18 30/05/2014 16:18 367 MOOD DISTURBANCE/PSYCHOSIS Depression1 Depression is low mood that is not usual and persists for over 2 weeks. It can be a symptom of other psychiatric disorders (eg bipolar disorder, personality disorders) or a disease in its own right.2 Symptoms low mood, low energy, feeling worthless or guilty, p oor con- centration, recurrent thoughts of suicide or death, low self-esteem, tearfulness, loss of interests, anhedonia; somatic symptoms weight/ appetite loss, sleep problems (early morning wakening, insomnia or excess sleeping), loss of libido, psychomotor agitation or r etardation, change in mood with time of day psychotic symptoms delusions, hallucinations. S igns neglect, agitation, slowed speech or movement, poor eye contact. Bereavement avoid dia gnosing within 2mth of bereavement; be aware of cultural variation in grief reactions; feat ures pointing to depression include prolonged, severe functional impairment or psychomotor retardation. Investigations often none; consider an organic cause and investigate if suspec ted, otherwise initiate treatment and review if not working. Treatment \200 Psychotherapy usually cognitive \200\223behavioral therapy (CBT) but interpersonal therapy (IPT) may also be eff ective; can be used with or without medications Antidepressants: fi rst line: selective serotonin re-uptake inhibitors (SSRIs) eg citalopram, fl uoxetine if a patient does not respond to SSRIs liaise with a psychiatrist about which medications to recommend; this may be second-line antidepressants, eg venlafaxi ne, mirtazapine or augmentation with lithium Electroconvulsive therapy (ECT) is considered if the patient is at high risk (eg not eating or drinking) and/or has failed to respond to medications. Prognosis outcome is generally good with the following: young, somatic symptoms, reactive d epression (due to a life-event) and acute onset. Complications deliberate self-harm, unempl oyment, relationship break- down, recurrence, suicide. Starting an antidepressant medication \200 Antidepressants generally start to work by 2 \200\2233wk but can take up to 6wk \200 Suicide risk may increase over the fi rst few wee ks \200 Antidepressants are generally well tolerated; side eff ects are usually mild \200 Treatment should continue for at least 6mth after the symptoms have resolved Antidepressants should be gradually weaned rather than stopped abruptly. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG90 2 A depressive episode is classifi ed by DSM-5 as minor or major and may be associated with somatic symptoms or psych otic symptoms; major depressive disorder is the recurrence of major depressive episodes wit hout mania; ICD-10 use the terms mild, moderate and severe, adding recurrent if more than o ne episode without mania. See box b p161 for details of the DSM-5 and ICD-10 classifi catio n systems. _OHFP.indb 367 _OHFP.indb 367 30/05/2014 16:18 30/05/2014 16:18 368 CHAPTER 11 Neurology and psychiatry Schizophrenia1 A chronic illness characterized by psychotic symptoms lasting over a month. Acute presentations are often characterized by positive symptoms; negative symptoms can per sist despite treatment. Positive symptoms delusions, hallucinations (often auditory): see f i rst-rank symptoms box. Negative symptoms blunted aff ect, apathy, loss of drive, social w ithdrawal, social inappropriateness, poverty of thought/speech, cognitive impairment. Signs neglect, disorganized behavior, paranoia. Investigations blds FBC, U+E, LFT, Ca2+, glucose , consider TFT, VDRL, cortisol; urine toxicology; EEG; CT/MRI. Treatment all people with a fi rst presentation should be urgently referred to a mental health team either in the commu nity (eg crisis resolution or home treatment team) or in secondary care depending on the se verity of episode (risk to self: suicide, job, assets, relationships and others). Antipsych otic medications (neuroleptics) are the mainstay of acute and chronic treatment: \200 Aty pical antipsychotics have less extrapyramidal side eff ects and a better eff ect on negativ e symptoms eg amisulpride, olanzapine, risperidone, quetiapine, clozapine; these are the pr eferred treatment in newly diagnosed schizophrenia, and for those experiencing side eff ect s or relapse on conventional antipsychotics Conventional antipsychotics eg chlorpromazine, haloperidol, trifl uoperazine, fl upentixol. Clozapine is a 3rd-line antipsychotic, used in treatment-resistant schizoph renia. It can c ause potentially fatal agranulocytosis; monitor FBC weekly for the 1st 18wk of treatment, 2 wkly for the next 34wk, and 4wkly thereafter. Side eff ects of antipsychotics include sedation, anticholinergic eff ects (eg dry mouth, b lurred vision, constipation), extrapyramidal side eff ects (eg parkinsonism) and tardive dy skinesia (late onset oral grimacing and upper limb writhing). Procyclidine may be used to r educe Parkinsonism. Complications deliberate self-harm, unemployment, relationship breakdow n, drug side eff ects, suicide. First-rank symptoms2 Delusions Delusional perception Passivity Passivity of thought, feelings or actions Hallucinations Thought \202 ow and possession Thought echo (audible thoughts) Thought withdrawal Third-person auditory hallucinations Thought insertion Running commentary Thought broadcasting In the absence of organic pathology, the presence of these features is suggestive, but not diagnostic of schizophrenia 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG178 2 Originally described by Kurt Schneider, a leading German psychiatrist, in 1959. OHFP.indb 368 OHFP.indb 368 30/05/2014 16:18 30/05/2014 16:18 369 MOOD DISTURBANCE/PSYCHOSIS Anxiety disorders/neuroses1 It is normal to have a degree of worry or fear. However if this causes distress or interferes with life then it is considered abnormal. There are several types of anxiety- and stress-related disorders: \200 Specifi c phobic fear of a specifi c situation or object, eg fl ying, spiders \200 Social phobia fear in social situations, e g public speaking \200 Panic attack excessive fear without any obvious trigger; associate d with symptoms of autonomic arousal, eg sweating, dizziness, nausea, palpitations, breathles sness; usually lasts <30min Panic disorder recurrent panic attacks with fear of having another \200 Generalized anxie ty disorder (GAD) excessive worry in everyday life \200 Obsessive \200\223compulsive diso rder (OCD) obsessive thoughts, eg \200\230my hands are dirty \200\231 leading to compulsions, eg repetitive hand washing. Symptoms worry, irritability, fear, avoidance of feared situations, checking, seeking reass urance, tight chest, shortness of breath, palpitations, \200\230butter- fl ies \200\231, t remor, tingling of fi ngers, aches, pain. Signs tremor, iHR, iRR; be careful to exclude any organic causes of symptoms such as breathlessness, chest pain or palpitations. Investigati ons consider FBC, U+E, LFT, Ca2+, cardiac markers, TFT, glucose; urinary VMA; ECG to exclud e organic causes of symptoms. Treatment careful explanation of the cause of their problems; relaxation techniques, psychological therapies, eg CBT; medications, eg SSRIs; benzodi- az epine use should be avoided in panic disorder and used only for <4wks in GAD, as these have poor long-term benefi ts and carry a risk of dependence. g y Relaxation techniques \200 Breathing exercises (silently counting breaths up to 10) \200 Visualization techniques (imagining a place, color, or image that is calming) \200 Prog ressive muscle relaxation (tensing and relaxing muscle groups in turn) \200 Relaxation CD s \200 Yoga. Personality disorders Ingrained patterns of behavior manifesting as abnormal and infl exibl e responses to a broad range of personal and social situations; the diagnosis is to be avoi ded in adolescents when the personality is still developing. Classi \201 cation DSM-V divi des personality disorders into 3 clusters: type A (odd, eccentric; includes paranoid); type B (dramatic, emotional; includes antisocial and borderline); type C (anxious, fearful; inc ludes dependent). Investigations usually none, but they require careful assessment over mul - tiple occasions and the exclusion of other psychiatric diagnoses. Treatment personality d isorders are challenging to treat. Psychotherapies may be useful, including dialectical beh avior therapy, cognitive \200\223analytical therapy, CBT, and psychodynamic psychotherapy. Antidepressants, mood stabilizers, and antipsychotics may also be used though the evidence of benefi t is limited. Complications suicide, self-harm, social isolation. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG113 _OHFP.indb 369 _OHFP.indb 369 30/05/2014 16:18 30/05/2014 16:18 This page intentionally left blank Chapter 12 Fluids and renal 371 Acute kidney injury 372 Chronic renal failure 373 Haematuria 374 Proteinuria 375 Glomerular disease 376 Urological disorders 377 Low urine output 378 IV fl uids 380 Potassium emergen cies 384 Electrolyte imbalance 385 _OHFP.indb 371 _OHFP.indb 371 30/05/2014 16:18 30/05/2014 16:18 372 CHAPTER 12 Fluids and renal Acute kidney injury 1 Acute rise from baseline of serum urea and creatinine oliguria (Tab le 12.1);1 there are three basic mechanisms: \200 Prerenal hypoperfusion of kidney due to eg dBP, hypovolaemia, renal artery occlusion (mass, emboli) Renal intrinsic renal pathology eg glomerulonephritis, vasculitis, drugs \200 Obstruction of outfl ow tract (ureter, bladder, urethra) by, eg enlarged prostate, single functioning kidney with calculi, pelvic mass or surgery. Acute tubular necrosis refers to irreversible renal damage with nephron loss that may occur due to prerenal or renal triggers eg due to prolonged hypoperfusion or nephrotoxic drugs ( NSAIDs, gentamicin, IV contrast). 3Call for senior help early. Table 12.1 Features of diff erent types of renal failure Prerenal hypoperfusion Acute tubul ar necrosis Renal Obstruction Oliguria, urine osmolality >500mOsmol/kg, urine Na+ <20mmol/l2 Oliguria/normal/polyuria, ur ine osmolality <350mOsmol/ kg, urine Na+ >40mmol/l2 Oligo/anuria, haematuria, iBP Oligo/anu ria, hydronephrosis on USS; if urethral: painful anuria with palpable bladder Oliguria/norm al/polyuria, previous icreatinine, dHb, dCa2+, iPO4 3 \210\222, small kidneys on USS, fatig ue, nocturia Chronic renal failure History previous renal or other medical problems, urine output, fl uid intake, medications (?nephrotoxic), rashes, bleeding, lethargy, anorexia. Examination volume status (b p380), B P (compare to what is normal for patient from eg old obs charts), HR, JVP, basal creps, gal lop rhythm, oedema, palpable bladder. Investigations urine color, hourly volume, dipstick, M,C+S, osmo- lality and Na+ (b p590); blds FBC, U+E, LFT, CK, CRP, osmolality, ESR, clottin g; ABG beware acidosis or iK+; urgent ECG iK+ causes fl at P waves, wide QRS and tall, peak ed T waves; CXR, urinary tract USS. Treatment insert catheter (b p546) to monitor output; a ssess for and treat causes and serious complications: \200 Obstructed catheter will relie ve urethral obstruction; ureteric obstruction may require nephrostomy or stenting Shocked iHR, dBP, absent JVP; fl uid resuscitate (b p472) inotropes \200 Overloaded oed ema, basal creps, iJVP: O2, furosemide (b p200), CXR \200 Hyperkalaemia insulin/glucose, Ca2+ gluconate, salbutamol (b p384). Continue IV fl uids unless overloaded (no KCl if iK+), stop nephrotoxic drugs (b p172) \200\223 this includes ACEi/metformin even if CCF/DM; mon itor urine output; consider HDU referral for CVP monitoring. 1 May be defi ned as any of: i creatinine of \211 26 mol/l in \211 48h, or \211 50% in 7d (if recent bloods unavailab le consider baseline values plus clinical history); or durine output <0.5 ml/kg/h for >6h ( adults) or >8h (children); or \211 25% deGFR in 7d (children only).NICE guidelines availab le at (cid:27)guidance.nice.org.uk/CG169 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 necrosi s, concentrating ability is lost. Calculating the fractional excretion of sodium (FENa) cor rects for dilution by relating sodium concentrations to creatinine (Cr): FENa = (UrineNa/Pl asmaNa)/ (UrineCr/PlasmaCr) X 100. FENa>1% supports a diagnosis of ATN. OHFP.indb 372 OHFP.indb 372 30/05/2014 16:18 30/05/2014 16:18 373 CHRONIC RENAL FAILURE Chronic renal failure 1 Long-standing and irreversible reduction in GFR. Causes DM, iBP, ch ronic urinary retention, glomerulonephritis, nephritis, pyelonephritis, polycystic kidneys, vasculitis. Symptoms initially none; tiredness, weight loss, nausea. Signs initially none, may have signs of causative disease eg DM. 3 \200\223, persistent pro- Results iurea, icre atinine, deGFR2, dHb, dCa2+, iPO4 teinuria and/or haematuria, abnormal/small kidneys on USS ; biopsy some- times necessary when cause unclear. Treatment involves regular review by a n ephrologist. Tight control of BP and DM, smoking cessation, ACEi and avoidance of nephrotox ins slows the pro - gression to ESRF. Management of complications includes cor rec - tion o f anemia with iron infu- sions erythropoietin, dietary and oral Ca2+ modi fi cation 3 \210\222 binders sup plements/PO4 to 3 \210\222, control prevent dCa2+/iPO4 of secondary hy perparathyroidism with vitamin D analogs. As the patient nears chronic kidney disease stage 5 (CKD 5 \200\223 see Table 12.2), wishes and suitability for dialysis and transplantatio n should be discussed and necessary arrangements made (eg dialysis counseling, fi stula cre ation). Complications vascular disease, anemia, dCa2+, renal osteodys- trophy, iK+, fl uid overload, immune compromise, peripheral neuropathy. Prescribing see b p172; avoid nephrotox ic drugs (eg metformin, NSAIDs, gentamicin); reduce doses/frequency of renal excreted drugs (eg opioids, benzodiazepines, penicillins); see also b p380 for fl uids. Radiology avoid I V contrast imaging except in emergency since this is nephrotoxic; discuss carefully with ne phrology and radiology. Where essential, use IV hydration and monitor renal function closel y. Table 12.2 Stages of CKD3 eGFR (ml/min) Stage >90 60 \200\22389 45 \200\22359 30-44 15 \200\22329 <15 1 2 3a 3b 4 5 (ESRF) 3 Reduction in eGFR needs to be sustained (eg \211 3 mth) and accompanied by evidence of renal disease (eg structural abnormalities, per sistent haematuria, proteinuria or microalbuminuria) Patients on dialysis Approximately 15,000 UK patients are on haemodialysis, usually for 3 \200\2235h 3x/week via an arteriovenous (AV) fi stula. Blood tests and BP measure- ments sh ould never be made from a fi stula arm. Placing fi ngers or a stetho- scope bell gently ove r a fi stula will confi rm function if a gentle buzz is felt or heard. A further 5000 UK pa tients use peritoneal dialysis via an abdominal (Tenckhoff ) catheter. Peritoneal infection s in these patients can be devas- tating; if septic, a sample of dialysate should be inspec ted (?turbid) and sent for cell count, Gram stain and culture; intraperitoneal antibiotics may be required. Always inform the renal team. 1 NICE guidelines available at (cid:27)guidance.nice.org.uk/CG73 See also the UK renal asso ciation website (cid:27)www.renal.org/home.aspx for useful educational material and links. 2 There are various methods of giving an estimated GFR (eGFR). Most labs use variations on the formula developed by the Modifi cation of Diet in Renal Disease (MDRD) study group whic h combine demographic data (age, sex, race) and serum chemistry (usually just creatinine). Original paper: Levey, A.S. et al. Ann Intern Med. 1999 130:461 available at (cid:27)annals .org/article.aspx?articleid=712617 (subscription required \200\223 check ATHENS) _OHFP.indb 373 _OHFP.indb 373 30/05/2014 16:18 30/05/2014 16:18 374 CHAPTER 12 Fluids and renal Haematuria Worrying features weight loss, frank blood or clots (?malignancy); iBP, proteinu ria (?nephritic syndrome b p376). Think about macroscopic UTI, tumors, stones; microscopic with red cells UTI, bladder, renal or prostate tumor, stones, recent catheterisation, glomerulonephritis/nephritic syndrome, endocarditis, clotting abnormality, sickle cell, TB, schistosomiasis, trauma, strenuous exe rcise, PV bleeding (b p496); microscopic without red cells (haemoglobinuria) haemolytic ane mia, myositis, rhabdomyolysis, trauma, ischaemia; red discolouration rifampicin, beetroot. Ask about urine color and volume, clots, dysuria, frequency, urgency, fever, abdominal pain , hesitancy, poor stream, recent trauma or catheteri- sation, weight loss, malaise, letharg y, menstruation; PMH kidney disease, stones, prostate disease, cancer, clotting disorders, sickle cell; DH nephro- toxic drugs (eg NSAIDs, gentamicin), rifampicin, anticoagulants. Ob s BP, HR, temp, fl uid balance. Look for iBP, haematuria and proteinuria suggest nephritic syndrome (b p376); inspect the urine; rashes, bruises, splinter hemorrhages, palpate for su prapubic or loin tenderness or masses; PR: enlarged prostate; PV bleeding. Investigations u rine dipstick may not distinguish red cells and haemo- globin, microscopy (for red cell or protein casts), culture; blds FBC, U+E, LFT, Ca2+, ESR, CRP, clotting; consider G+S, autoan tibodies (anti-GBM, ANCA, ANA, anti-DNA), complement, PSA, USS urinary tract. Management Ma croscopic (red/pink urine) resuscitate (b p478), if heavy consider inserting a three-lumen 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