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Long-term neurological conditions Chapter 7: Neurology 115
https://t.me/med1917
Secondary headaches
THUNDERCLAP HEADACHE
Symptoms:
S: Back of head / occipital
O: Sudden, peaks intensity in <1min
C: Like a blow to the head
A: Vomiting, neck stiffness
± subhyaloid (intraocular) haemorrhage
Investigations: urgent CT
If CT is negative = lumbar puncture
→ Look for xanthochromia in CSF
→ Must be ≥12h after headache onset but not useful after 2–3w
RAISED ICP HEADACHE
Symptoms:
S: Whole head / occipital area
O: Days to weeks
A: Papilloedema, focal Sx if mass lesion, transient visual obscuration
T: Progressively worsening
E: Bending, coughing, exertion, in mornings
Investigations: urgent CT/MRI & CT/MRI venograms
→ Check BP
→ If CT/MRI normal, LP to check opening pressure
Management: urgent neurosurgical referral
Differentials of thunderclap headache:
• Migraine
• Meningitis
• Coital headache – much briefer (30–60min)
& recurrent
• Venous sinus thrombosis
• Reversible vasoconstriction syndrome
→ following steroids / nasal decongestants
→ Dx with CT angiogram
Differentials/causes of raised ICP headache:
• Mass lesion
• Hydrocephalus
• Venous sinus thrombosis
• Idiopathic intracranial hypertension (IIH)
Risk factors for IIH:
SAH until proven otherwise
female, BMI, tetracycline, OCP
LOW PRESSURE HEADACHE
Cause: spinal CSF leak (can be due to epidural / spinal tap / penetrating wound,
trauma, spontaneous)
Symptoms:
S: Whole head / occipital area
O: Days to weeks (can pinpoint starting day)
A: Neck pain, nausea, hearing change, imbalance
T: Progressively worsening
E: Being upright (absent when supine)
Investigations: urgent CT/MRI head & spine
Management:
1st line: bed rest + fluids + caffeine
2nd line: blood patch
GIANT CELL ARTERITIS HEADACHE
Symptoms:
S: Temporal/occipital
O: Acute
A: Jaw claudication, scalp tenderness, polymyalgia rheumatica, weight loss,
vision changes
Investigations: urgent as risk of blindness
→ CRP/ESR
→ Temporal artery biopsy
Management: high dose prednisolone + ophthalmology referral if eye symptoms
tends to affect those >50y
Differentials of GCA:
• Migraine
• Stroke
Medicine
https://t.me/med1917
inhibitor
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117
antibody
rate
118 Chapter 8: Renal
https://t.me/med1917
Incidence: common
10–20% hospital admissions
20–30% cardiac surgery patients
50% ICU admissions
→ Address RFs in hospitalised patients to
prevent AKI
KDIGO staging of AKI1
Stage Serum creatinine Urine output
<0.5ml/kg/h for 6–12h
>26.5µmol/L within 48h
<0.3ml/kg/h for >24h
>353µmol/L OR
requiring renal replacement therapy
OR
Anuric for >12h
Classication of AKI
Pre-renal
Causes Volume depletion:
• Blood loss / dehydration / burns
Reduced BP:
• Shock / cardiogenic shock
• Medications
Reduced vascular perfusion:
• Renal artery stenosis
Renal vasoconstriction:
• ACEi/NSAIDs
Intra-renal
Vascular:
• Vasculitis
• HUS
Glomerular: glomerulonephritis
(e.g. immune-mediated vasculitis)
Tubular disease:
• ATN (if persistent perfusion)
• Multiple myeloma
• Rhabdomyolysis
Interstitial nephritis:
Post-renal
Intrinsic obstruction:
• Malignancy
• Stones
• Stricture
Extrinsic compression:
• BPH
• Pelvic malignancy
• Retroperitoneal fibrosis
Acquired:
• Blocked catheter
• New drug (hypersensitivity)
Urine dip No blood, no protein Blood ± protein Blood or leucocytes
No protein
Urine osmolality (osm) Can retain Na to concentrate urine
= urine osm high, urine Na low
Cannot retain Na / concentrate urine
= urine osm low, urine Na high
Cannot concentrate urine if
kidney damage
= urine osm low/normal
Symptoms
Vague & non-specific → arise due to biochemical disturbances
• Oliguria/anuria • Abdo pain • Dizziness, headache • Nausea, vomiting
± Signs of dehydration
± Signs of vasculitis (rash etc.) ± Abdo distension
± Signs of shock
Management
2
1. ABCDE – ABX if septic
2. Stop nephrotoxic drugs
3. Assess & manage fluid status – BP, pulse, HR, mucous membranes
Regular monitoring:
U&Es, BP, ABG
4. Assess & manage electrolyte imbalances – daily U&Es, ECG
Volume replacement (IV fluids) if
volume depletion
Consider fluid restriction & loop diuretic if
overloaded
1. Consider urine drainage/catheter
2. Refer to urology
Medicine
1
KDIGO (2012) Clinical Practice Guideline for Acute Kidney Injury. Kidney Intl, 2(Suppl 1)
2
NICE (2019) Acute kidney injury [NG148]
Risk factors for AKI
https://t.me/med1917
impairment
penicillins, lithium, contrast medium
Chapter 8: Renal 119
Complications of AKI
• Hyperkalaemia
• Fluid overload
• Pulmonary oedema
• Metabolic acidosis
• Uraemia
Indications for dialysis: Life-threatening, refractory AKI with complications
• Severe hyperkalaemia/acidaemia/uraemia
• Refractory pulmonary oedema
• Toxins/drugs
Investigations
1. History & examination
→ Risk factors for AKI → ‘VENUS’
→ Symptoms suspicious of glomerulonephritis/vasculitis
→ DRE for enlarged prostate
2. Urine dip to r/o UTI & determine if underlying glomerular disease
→ if no blood or protein – pre-renal or tubulointerstitial cause
→ if blood & protein – renal cause
→ if blood only – post-renal or renal cause
→ if nitrites ± leukocytes – need to r/o infection → MCS
3. Further urinalysis: MCS, casts, Bence Jones protein (if suspect myeloma
e.g. high calcium)
3
Severe hyperkalaemia (>6mmol/L)
Symptoms:
Chest pain, palpitations, dizziness
Investigations:
U&Es, fluid balance, ECG
Management:
1. 10ml 10% calcium gluconate = stabilise
2. IV insulin + 25g glucose = drive potassium
3. Salbutamol nebs = drive potassium into cells
4. 1.4% sodium bicarbonate = correct acidosis
5. Treat cause
• Haemolysis, haemoptysis, hypercalcaemia
• Rash, raised CK, recent vascular intervention
oliguria)
4. Bloods: need to know baseline (review previous creatinine)
→ FBC – raised CRP/ESR if infection/inflammation
→ U&Es – raised Cr, urea, K+, Na
→ nephritic screen – if unexplained AKI/CKD or features suggesting vasculitis
5. Arterial blood gas – if severe acidosis, consider overdose
6. ECG – signs of hyperkalaemia (flat P, broad QRS, tented T)
7. Renal USS or CT KUB – may show signs of obstruction
(hydronephrosis, distended bladder, stones)
3
Nitin, et al. (2016) A simple care bundle for use in acute kidney injury: a propensity score-matched
cohort study, Nephrol Dial Transplant, 31:1846
+
• ANCA (vasculitis)
• ANA/ds DNA (SLE)
• Complement (low in infection/SLE)
• Hepatitis B and C serology
Medicine
120 Chapter 8: Renal
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Factors increasing risk of needing RRT
Classication
• Younger age
• Lower eGFR
• Male gender
• Higher ACR
Signs/symptoms:
• Anaemia: pallor, fatigue
• Bone disease: osteomalacia/fractures
• Hyperkalaemia: palpitations, dizziness,
chest pain
• Fluid overload: peripheral oedema, SOB
• Early uraemia: fatigue, anorexia, N&V,
pruritus, hiccups
• Late uraemia: confusion
• Metabolic acidosis: HR & RR, vomiting,
fatigue, headache
• Other: sexual dysfunction = common
** CKD associates with cardiovascular events
& AKI **
Investigations:
1. Urine dip & BP
→ Urine protein–creatinine ratio
for nephrotic syndromes
→ Urine albumin–creatinine ratio (ACR)
for CKD
2. Bloods:
→ U&Es – compare to previous eGFR
→ Bicarbonate – acid–base balance lost
→ Hb – normocytic anaemia
→ PTH ( if bone disease & also ALP)
→ Glucose (for DM)
→ ANA, ANCA, complement
3. USS kidney (kidneys may be small)
4. Renal biopsy – if still unsure of cause
5. CXR – for pulmonary oedema
Base on 2 factors:
1. GFR
2. Albuminuria
Persistent albuminuria
A1 A2 A3
<3mg/mmol 3–30mg/mmol >30mg/mmol
GFR (ml/min/1.73m2) G1 ≥90
G2 60–89
G3a 45–59
G3b 30–44
G4 15–29
G5 <15
Table based on KDIGO AKI staging system.
Causes of deteriorating GFR
Diabetes mellitus (38%)
Hypertension (25%) Thickened walls of afferent arteriole = hypoperfusion
Chronic glomerulonephritis (16%) Inflammation & damage to vessels
Chronic pyelonephritis Urinary reflux or recurrent infection
Obstructive uropathy Back-up of pressure = hydronephrosis & damage
Polycystic kidney disease (PKD)
Management of CKD
1. BP control: ACEi/ARB if proteinuria (BP<140/90 or <130/80 if diabetic)
2. Cholesterol control: statin
3. Comorbidity control: diabetes control
4. Stop smoking
5. Weight management
Glycation of efferent arteriole = pressure & sclerosis
→ neurogenic bladder, BPH, malignancy, stones
→ Auto dominant form presents in adults
→ Fluid-filled cysts press on nephrons = atrophy
→ Sx: back pain, headaches, haematuria, HTN
4
Advise low salt & phosphate diet
Pathogenesis of renal bone disease:
Vit D activation in kidneys = Ca absorption
= 2° hyperparathyroidism ( PTH)
PTH causes osteoclastic activity
= Ca resorption from bone to restore serum Ca
= leaves bone weak
In kidney transplant patients, parathyroid
gland may become autonomous in spite
of normal renal function = tertiary
hyperparathyroidism
Medicine
1. Anaemia – IV iron + EPO stimulating agents (r/o B12/folate deficiency first)
2. Bone disease – vit D & calcium supplements if deficient, phosphate binders
3. Oedema – careful fluid monitoring ± diuretics
4
NICE (2021) Chronic kidney disease [NG203]
1. Stop drugs that worsen glomerular function / acute nephrotoxics
https://t.me/med1917
2. Alter dose of medications if GFR is low e.g. stop metformin if GFR <30
→ assess & manage symptoms/complications & prep for RRT
Renal replacement therapy options
Haemodialysis Peritoneal dialysis
Method Blood pumped out of body
through ‘artificial kidney’
Access AV fistula / semi-permanent
jugular or subclavian catheter
Complications Site infection, hypotension,
air embolus, N&V, endocarditis
Frequency 3 × 4h sessions each week Continuous ambulatory = 4 × 20min each
Dialysate solution infused into peritoneal cavity
(peritoneum acts as filtering membrane)
Catheter into peritoneum
Peritonitis, catheter problems, hernia, fluid
retention, weight gain
day while active
Automated = overnight (3–5 exchanges over
8–10h)
Chapter 8: Renal 121
ensure patients are fully informed of all options &
supported in decision-making
→ but only 40% of patients with CKD 5 are suitable
Process:
→ Transplant placed in iliac fossa & anastomoses of vessels made
→ Usually leave native kidney in place
Post-transplant treatment:
→ Lifelong immunosuppression = tacrolimus or ciclosporin plus azathioprine/
MMF
→ 6m of steroids to prevent acute rejection e.g. prednisone
→ Aspirin, antihypertensives, PPI, bone protection
Complications:
cardiac disease, infections
Ethical issue: waiting list of >4500 (avg. wait = 3y)
Pros Cons
• Longevity (80% 10y survival)
• Quality of life (free from dialysis)
• Medication burden
• Immunosuppressive SEs
• Frequent hospital visits
Who is suitable?
• Generally fit for general anaesthetic
• At least 5y left to live
• No underlying malignancy
• No other significant comorbidities
• Good vascular supply to legs
+ a suitable match is found:
→ ABO, tissue type, age & gender
Transplant rejection: 10–20%
→ Often asymptomatic (concern if rise in Cr)
→ RFs: non-concordance, drug interactions,
poor match
→ Tx: IV methylprednisolone &
immunosuppressants
5
Major, et al. (2019) The Kidney Failure Risk Equation for prediction of end stage renal disease in UK
primary care. PLOS Medicine, 16:e1002955
Medicine
122 Chapter 8: Renal
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Nephrotic syndrome
patients often report FROTHY URINE
→ immune complex deposition &/or complement activation
1. Minimal change disease = most common in children
• microscopically normal renal tissue
2. Focal segmental glomerulonephritis
• thickened BM & focal areas of sclerosis
• results in damage to podocytes
3. Membranous glomerulonephritis = 30% adult cases
• complement activation & IC deposition causes BM thickening & podocyte damage
• (anti-phospholipase a2 antibodies present)
1. Heavy proteinuria (>3.5g/d)
2. Hypoalbuminaemia (<25g/L)
3. Oedema – periorbital, legs, scrotal/vaginal
• Peripheral & periorbital oedema (loss of albumin)
• Pleural effusion (loss of albumin)
• Hyperlipidaemia (loss of liporegulatory proteins)
• Hypercoagulability (loss of thromboregulatory proteins)
• Infections (loss of immunoglobulins)
Primary
→ damage due to underlying disease
1. Diabetic nephropathy = most common cause
2. SLE
3. Infection: hepatitis B/C, HIV, malaria, syphilis
4. Drugs: penicillamine, gold, NSAIDs, iron
5. Amyloidosis
6. Myeloma
7. Pre-eclampsia
can also get haematuria
iflots of BM damage
Secondary
aim for 0.5–1kg weight loss per day
Confirming diagnosis
• Urine dip – protein
• Urine MCS – r/o UTI
• U&Es, Cr, albumin
• FBC, ESR/CRP, LFTs
• Renal biopsy – shows microscopic changes to glomeruli (confirms subtype)
Determine cause:
• Autoimmune screen (ANCA, anti-phospholipase a2, complement levels)
• Serum & urine immunoglobulins / electrophoresis
• Infection screen (throat swab / anti-strep, hep B & C, HIV, syphilis, malaria)
Assess complications:
• CXR – pleural effusion
• Lipid profile – loss of liporegulators in urine
• TFTs – loss of thyroid hormones in urine
• Coag screen – loss of thromboregulators in urine
1. Reduce oedema: loop diuretics + fluid & salt restriction (max 1L fluid/d)
2. Reduce proteinuria: ACEis/ARBs (cause efferent vasodilation)
3. Treat underlying cause: corticosteroids indicated in minimal change disease
Medicine
6
KDIGO (2021) Clinical Practice Guideline for the Management of Glomerular Diseases
Nephritic syndrome
https://t.me/med1917
Chapter 8: Renal 123
→ Inflammation damages glomerular capillary so RBCs leak into nephron
→ Inflammation damages podocytes allowing protein to leak into nephron
→ Inflammation causes reduced GFR, leading to oliguria & hypertension
1. Haematuria (>10 red cell casts)
2. Oliguria (<0.5–1ml/kg/h)
3. Proteinuria
• Volume overload / reduced GFR
▶ Oedema (esp. periorbital)
▶ Hypertension → seizures
• If severe presents as AKI: oliguria
1. Autoantigens (Goodpasture’s disease): anti-BM antibodies (often also get
alveolar haemorrhage & haemoptysis)
2. ANCA-associated (small vessel vasculitis): p-ANCA & c-ANCA activate
macrophages & neutrophils = immune damage
▶ Prodrome of malaise, arthralgia/myalgia, skin rash & AKI
▶ No immune complex deposition seen
3. Immune complexes: immune complex deposits activate complement &
inflammation
▶ Results in low complement
▶ Causes*: IgA nephropathy, post-strep infection (HSP) & SLE
*Any of these can lead to rapidly progressing glomerulonephritis & acute
renal failure
• Often low complement
• Check for ANCA, ANA & anti-strep
1. Goodpasture’s disease: plasmapheresis (removes Abs), corticosteroids,
cyclophosphamide (immunosuppressant)
2. ANCA-associated vasculitis: induce remission with corticosteroids &
cyclophosphamide → maintain with azathioprine
3. IgA nephropathy / post-strep infection: ACEi/ARB (protect renal function),
± corticosteroids
RBCs clump together = casts
GLOMERULONEPHRITIS:
causing immune-mediated inflammation of
glomerulus (= permeability)
= Spectrum of nephrotic & nephritic
syndromes
• Post-infections (malaria/staph/salmonella/
strep)
• Systemic autoimmune diseases / vasculitis
e.g. SLE
• Proteinuria & haematuria
• Features of systemic autoimmune vasculitis
(sweats, weight loss, arthralgia, eye signs, rash,
mouth ulcers)
• Diuretics if nephrotic component – maintain fluid & electrolyte balance
• Treat infection if present – ABX (penicillin)
• If rapid renal function: renal biopsy, immunosuppression, plasma exchange
• Diuretics ± steroids ± ABX
Medicine
124 Chapter 8: Renal
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Clinical presentation
Risk factors for UTI:
• Female
• Sexual intercourse
• Pregnancy
• Diabetes
• Dehydration
• Immunosuppression
• Incomplete
emptying
• Structural
abnormality / reflux
• Instrumentation
(e.g. catheter)
(e.g. ABX)
Common organisms:
1. E. coli = 85%
2. Staph. saprophyticus = 5–10%
3. Enterococci
↳ in young / sexually active
4. Proteus
5. Klebsiella
6. Pseudomonas if catheter
DO NOT urine dip if >65y, send straight
for MCS
Upper (pyelonephritis)7Lower (cystitis)8
Symptoms • Dysuria (burning)
• Frequency/urgency
• Flank/loin pain
• High grade fever, N&V
• Dysuria (burning)
• Frequency/urgency
• Suprapubic pain
• Foul-smelling, cloudy urine
• ± Haematuria
Investigations 1. Urine dip: leukocytes (sensitive), nitrites (specific)
2. MSU for MCS: confirm Dx (>105 WCC/ml)
3. Bloods: FBC, CRP/ESR, U&Es, culture (if systemically unwell /
pyelonephritis)
4. USS KUB: if recurrent, Tx-resistant or male
Management 1. Admit
2. Analgesia
3. IV ABX: ciprofloxacin or
cefuroxime (7d)
1. Lifestyle: hydration, personal hygiene
2. Analgesia: NSAIDs, paracetamol
3. ABX: trimethoprim or nitrofurantoin
→ Women: 3d course → Men: 7d course
Do not treat asymptomatic bacteriuria unless pregnant
Urinary tract TB: sterile pyuria with urinary Sx + fever, sweats, weight loss
Pseudo-haematuria:
• Menstruation
• Dyes/food
• Drugs (rifampicin)
Summary of causes of haematuria:
• UTI
• Stones
• Trauma
• Malignancy
• BPH
• Iatrogenic
Classication
• Microscopic or macroscopic
• Asymptomatic or symptomatic (associated with other urinary symptoms/pain)
Causes
Upper urinary tract Lower urinary tract
Kidney Ureter Bladder Prostate Urethra
• UTI
• Stones
• Trauma
• Cancer (RCC
or TCC)
• Cancer (TCC)
• Stones
• UTI
• Stones
• Trauma
• Cancer (TCC)
• Iatrogenic (catheter)
• BPH
• Adenocarcinoma
• Cancer
• Trauma
Investigations
1. Hx & exam: remember DRE
2. Urinalysis: dip & MSU
3. Bloods: FBC, clotting, U&Es, PSA
4. Renal USS: show calculi
5. Flexible cystoscopy: show bladder/urethral abnormalities
6. CT KUB: gold standard → if suspicious of cancer / recurrent haematuria
Medicine
7
NICE (2018) Pyelonephritis (acute) [NG111]
8
NICE (2018) Urinary tract infection (lower) [NG109]
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