Transcript Dizziness | Vertigo

CES: Genitourinary System
Tom Heaps
Consultant Acute Physician
Outline

Basic anatomy

Functional physiology

Symptoms

Examination

Nephrolithiasis

Obstruction
BREAK
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Acute Kidney Injury (AKI)
Basic anatomy
Kidneys
Ureters
Bladder
Urethra
Functional anatomy
Outer cortex
Inner medulla
Nephron
Calyces
Renal Pelvis
Ureter
Nephron: the functional unit of the kidney
Glomerular filtration
Net filtration pressure at the glomerulus
= blood hydrostatic pressure – colloid oncotic pressure – capsular hydrostatic pressure
= 55mmHg – 30mmHg – 15mmHg
= 10mmHg

Large surface area and porous membrane

glomerular filtration rate (GFR) of 125 mL/min in normal health

fluid volume of ~180L/day enters glomerular capsule
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GFR is regulated by the body depending on circulating volume and [Na+]
Filtration
Vasoconstriction
mediated by
angiotensin II
Vasodilatation
mediated by
prostaglandins
 Glomerular

hydrostatic
pressure and
filtration
NSAIDs reduce
prostaglandin
synthesis
ACE-inhibitors reduce
production of
angiotensin II from
angiotensin I by ACE
Role of the kidneys
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Production and excretion of urine
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Removal of waste e.g. creatinine, urea, uric acid
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Maintenance of homeostasis
Regulation of ECF volume and composition:

Control of ion balance and pH
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Control blood volume / blood pressure

Control osmolality (excretion / resorption of Na+)
Production of hormones / vitamins

Renin and erythropoietin (EPO)

Vitamin D3
GU Symptoms 1
Too much urine
DM, DI, hypercalcaemia, postobstruction
Not enough / no urine
Dehydration , AKI, obstruction
Going too often
Infection, stones, detrusor
instability
Urgency
Having to go quickly!
Infection, detrusor instability
Dysuria
Painful / burning micturition
Infection
Nocturia
Going >2x per night
Outflow obstruction, infection,
stones, detrusor instability,
causes of polyuria
Hesitancy
Difficulty starting
Outflow obstruction
Terminal Dribbling
Weak stream
Outflow obstruction
Incontinence
Loss of control
Urge, stress, neurological
problems, dementia
Polyuria
Oliguria / Anuria
Frequency
GU Symptoms 2
Infection, stones, tumours,
trauma, glomerulonephritis,
coagulopathy / anticoagulants
Haematuria
Microscopic or Macroscopic
Renal Angle Pain
Renal: pyelonephritis,
Non-renal: cholecystitis,
abscess, stones (renal colic), hepatitis, pancreatitis, splenic
hydronephrosis, cysts,
infarction, gynaecological,
tumours, infarction
shingles, basal pneumonia, MSK
Pain along the urethra +/discharge
Infection / urethritis, STI, stone,
foreign body, tumour
Orchalgia
Testicular pain
Epididymo-orchitis, tumour,
trauma, torsion
Prostatitis
Perineal pain, dysuria,
obstructive symptoms,
tenderness on DRE
Urogenital infection or
instrumentation
Urethralgia
Additional GU History

Hypertension, diabetes
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Family and congenital history
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Drug History

Sexual and travel history
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Systems review
GU Examination
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Full systems examination focusing on abdomen

Inspection
GU Examination

Full systems examination focusing on abdomen

Inspection

Palpation

Percussion

Auscultation
Costovertebral angle between lower border of 12th rib and
lateral border of erector spinae
Pain / tenderness, Murphy’s punch +ve
Kidneys usually not palpable unless hydronephrosis,
tumour, cystic disease
Palpate specifically for bladder distension in the elderly
GU Examination

Full systems examination focusing on abdomen

Inspection

Palpation

Percussion

Auscultation
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Perineum / Scrotum / Testicles
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Vagina / Penis
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Digital rectal examination (DRE)

Prostatic enlargement and / or tenderness

Constipation

Masses
Nephrolithiasis (urinary tract stones)
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>80% are calcium stones, majority of these are calcium oxalate
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Usually asymptomatic until they pass into ureter
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Pain (may be excruciating) and nausea

Waxing and waning (renal / ureteric colic)

Abdomen / flank  testicle / penis / labia (‘loin to groin’)

Haematuria, frequency, urgency, dysuria, strangury
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Non-contrast CT urogram is Ix of choice (sensitivity 88%, specificity 100%)
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USS if radiation an issue (sensitivity 57%)
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Plain AXR no longer has a role (if CT available)
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Conservative Rx with hydration, NSAIDs / opioids, tamsulosin / nifedipine
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Urgent urological referral if AKI, sepsis, stone >10mm
Urinary retention / obstruction
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Acute vs. chronic, unilateral vs bilateral
Kidney / ureter – stones, TCC, extrinsic tumour, retroperitoneal fibrosis
Bladder – stones, tumour, blood clots, neurological, drugs, constipation
Urethra – prostate cancer, BPH, stricture, stone
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Pain (may be absent in chronic retention and dementia)
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Oligo-anuria and AKI, haematuria, hypertension,
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DRE is mandatory, bladder scan then USS abdomen / pelvis
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IV fluids, urinary catheter, fluid balance, -blockers and antispasmodics
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Treat precipitant (pain, infection, constipation, drugs etc.)
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Be vigilant for post-obstructive diuresis and decompression haematuria

Other Rx e.g. ureteric stent, nephrostomy
Acute Kidney Injury
Tom Heaps
Consultant Acute Physician
Clinical Case

82-year-old male presenting with confusion and vomiting

PMHX: T2DM, hypertension, heart failure, BPH

DHX: Aspirin, metformin, ramipril, bendroflumethiazide, bisoprolol

RR 24, SpO2 94% (air), T 38.5C, BP 101/50mmHg, HR 119/min

Urine dip: leuc +++, nit +ve, blood +, protein ++

Na+ 144mmol/L

K+ 5.9mmol/L
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urea 15.4mmol/L
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creatinine 142μmol/L
With reference to this case…
GROUP 1: Is this AKI? What are the definitions of AKI?
GROUP 2: What are the risk factors for AKI? Which apply to this case?
GROUP 3: What are the common causes of AKI? Which apply to this case?
GROUP 4: What are the 6 most important steps in management of AKI?
GROUP 5: What are the complications of AKI and how are they treated?
AKI 1: definitions
calculated GFR is usually more accurate than serum creatinine in estimating
renal function but most definitions of AKI rely on creatinine measurement
KDIGO (Kidney Disease Improving Global Outcomes) definition of AKI:
 creatinine rise by ≥ 26µmol/L within 48 hours or;
Stage of AKI
Serum Creatinine (SCr) criteria
Urine output criteria
 creatinine rise ≥ 1.5-fold from the reference value* which is known or
presumed increase
to have occurred
within
one 48h
week
≥ 26 μmol/L
within
oror
<0.5 mL/kg/h for >6
1
increase ≥1.5x to 1.9x reference SCr
consecutive hrs
 urine output < 0.5mL/kg/h for >6 consecutive hours
2
increaseis≥the
2xlowest
to 2.9x
reference
SCr
<0.5 mL/kg/h
for >12 hrs
*reference
serum creatinine
creatinine
value recorded
within
3m of the event
3
increase ≥3x reference SCr or
increase ≥354 μmol/L or
commenced on renal replacement
therapy (RRT) irrespective of stage
AKI 2; risk factors
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CKD (especially if eGFR <60mL/minute)
heart failure
liver disease
diabetes
history of AKI
neurological / cognitive impairment or disability
hypovolaemia
use of drugs with nephrotoxic potential (NSAIDs, ACE-i, diuretics etc.)
use of iodinated contrast agents within the past week
symptoms / history of or conditions predisposing to urological obstruction
sepsis
deteriorating early warning scores (MEWS)
age ≥ 65
AKI 3: causes
Pre-Renal
Renal
Post-Renal (Obstructive)
(75%)
(20%)
(5%)
• hypotension
• hypovolaemia
• redistribution
• decreased cardiac
output
• renal artery stenosis
or thrombosis
• nephrotoxic
medications
• glomerulonephritis
• interstitial nephritis
• vasculitis
• ischaemia
• rhabdomyolysis
• urethral e.g. BPH
• bladder e.g. stones,
blood clots, tumours
• ureteric e.g. stones,
fibrosis, malignancy
• PUJ obstruction
• intra-tubular e.g.
crystals
• renal vein thrombosis
• abdominal
compartment
syndrome
AKI 4: management principles
1.
Treat underlying cause
IV fluids
 restore
and
renal
perfusion
(may require(CVVH)
vasopressors)
Haemodialysis
(HD)
vsmaintain
Continuous
Veno-Venous
Haemofiltration
 balanced crystalloids e.g. Hartmann’s + / - sodium bicarbonate
2.
Indications for Renal Replacement Therapy (RRT) in AKI
Prevention is better than cure…
55% of AKI is avoidable (including 30% of deaths due to AKI)
Myths
regarding
balanced

severe
refractory
metabolic acidosis
(pH <7.1, HCOcrystalloids…
<12 or BE < -10 )
4. Monitoring
3. Stop
nephrotoxics
and adjust
doses of other medications if necessary
persistent
hyperkalaemia
(K+ >7.0mmol/l)
3
-
 refractory pulmonary oedema
 strict
fluid
input
/ output
monitoring
‘
you
can’t
give
Hartmann’s
to
patients
with hyperkalaemia because
 uraemic complications (urea usually
>45mmol/L)
5.
 consider urinary catheter
it contains potassium’
 monitor for and treat complications of AKI
‘you can’t give Hartmann’s to patients with lactic acidosis because it
USS urinary tract
contains lactate’
selected cases only
6.
Renal referral + / - RRT
AKI 5: complications

hyperkalaemia (K+ >5.5mmol/L)

other electrolyte abnormalities e.g. hyperphosphataemia, hyponatraemia

metabolic acidosis
 IV fluids, IV bicarbonate (especially if hyperkalaemia), RRT

fluid overload / pulmonary oedema
 diuretic / GTN (often ineffective), RRT

uraemia: encephalopathy, pericarditis, bleeding

mortality
 overall mortality 26% (severity of illness and / or frailty of patient)
 16% in Stage 1, 33% in Stage 2, 36% in Stage 3, 58% if RRT required
QUESTIONS?