Block 3: heart transplant and AKI Flashcards

1
Q

What are the class 1 indications for cardiac transplant

A
  • Cardiogenic shock requiring mechanical assistance, refractory HF with continuous inotropic infusion
  • NYHF functional class 3 or 4 with poor 12 mn prognosis
  • progressive symptoms on maximal therapy
  • severe symptomatic hypertrophic or restrictive cardiomegaly
  • medically refractory angina with unstable anatomy for revascularization
  • life-threatening ventricular arrhythmias despite aggressive medical and device interventions
  • cardiac tumors with low likelihood of mets
  • hypoplastic left heart and complex congenital heart disease
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2
Q

What are some contraindications to cardiac transplant

A

1) Severe pulmonary HTN (>6 wood units not responsive to vasodilators)
2) active infection
3) uncontrollable malignancy
4) irreversible end-organ damage (hepatic, renal or pulmonary)
5) pulmonary infarction
6) age >60
7) diabetes mellitus with end-organ damage
8) severe cerebral or peripheral vascular disease

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3
Q

What blood tests should be done before a cardiac transplant

A

BMP, FBC, LFTs, UA, coags, TSH, UDS, ETOH level, HIV, hepatitis panel, PPD, CMV IgG, RPR/VDRL, PRA (panel of reactive antibodies), ABO and Rh blood type and lipids

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4
Q

What is the donor criteria for a cardiac transplant

A

Age <53 (<45 ideally), size- donor and recipient must have a size difference of <20kg. ABO blood type- <15% reactivity on the test allows transplant. >15% needs a lymphocyte cross-match test which takes 6 hrs and can delay the procedure. Brain death is required for any cadaveric organ donation- there should be no hypothermia, hypotension, metabolic abnormalities or drug intoxication

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5
Q

How do you match cardiac transplant

A

based on severity of disease, ABO blood type, response to PRA, donor recipient weight ratio, geographical location and length of time at current status

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6
Q

Immunosuppressants and cardiac transplant

A

Cyclosporine (and azothioprine)
Started on day of operative (IV then converted to PO 3 days later)

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7
Q

Types of cardiac transplant

A

Orthotopic (most common)- native heart is completely removed and replaced
biatrial anastomosis: recipient and donor atria are connected together
bicaval anastomosis- superior vena cava and ventricle are connected together
heterotopic heart transplant (2 hearts in the chest)

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8
Q

What investigations are used to check for rejection post cardiac transplant

A

Heart muscle biopsy (weekly for first 3-6 weeks, every 3 months for the first year, and then once a year)

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9
Q

What are the possible complications in cardiac transplant

A

Aortic pseudoaneurysm or rupture at cannulation site, or haemorrhagic pericardial effusion due to bleeding or coagulopathy. Medical- severe tricuspid regurg, RV failure (PA compression, PAH) or LV failure (ischaemia, operative injury and acute rejection). Rhythm disturbance- asystole, complete heart block, sinus node dysfunction with bradycardia (25% permanent, most resolve in 1-2 weeks), AF or VT. Coagulopathy induced by cardiopulmonary bypass. Resp failure- cardiogenic pulmonary oedema, noncardiogenic pulmonary oedema or infection. Renal or hepatic insufficiency- drugs or CHF

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10
Q

Types of cardiac rejection

A
  • Hyperacute: pre-existig IgG antibodies usually directed against donor HLA proteins. Occurs in mins-hours
  • Acute cellular rejection: most common in 2-3 months
  • Allograft vasculopathy/chronic rejection: coronary heart disease in transplanted heart from immune mediated injury
  • CMV is the most common infection transmitted
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11
Q

What is used to prevent chronic rejection in cardiac transplant

A

Immunosuppression, statins, diltiazem and antioxidant vitamins

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12
Q

Causes of death cardiac transplant

A
  • Most common cause of death: cardiac allograft vasculopathy (chronic rejection)
  • Most common cause of death in the first year after: acute rejection and infection
  • If a patient has N+V admit them so they can get their immunosuppressants UV
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13
Q

Indications for lung transplant

A

1) untreatable ESRD: pulmonary, parenchymal, or vascular
2) Absence of other medical illness
3) projected life expectancy < 2yrs
4) NYHA Class III or IV fuctional level
5) Forced expiratory volume FEV <30%
6) BODE < 5
7) PA pressure >50 mmHg
8) Rehabilitation potential
9) Acceptable nutritional status

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14
Q

Contraindications for lung transplant

A

Incurable malignancy, age >69, active or incurable infection- HIV, Hep C, other major organ system damage (kidney, liver), morbid obesity, alcohol, smoking or drug abuse, corticosteroid therapy, or revious CT surgery (case by case)

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15
Q

The requirements of a donor for lung transplant

A

<50, infection free, pO2 >140 on 40% O2 and pO2 >300 on 100% O2, peak inspiratory pressure <30cm H2O and smoking Hx <20 pack years with no COPD

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16
Q

Follow up needed for lung transplant

A
  • Lung biopsies at 2 and 4-6 weeks, 12 weeks, 6 months and then yearly.
  • Home spirometry daily and tacrolimus level, basic labs, CMV PCR and spirometry at each visit.
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17
Q

Complications for lung transplant

A

Short term: Bleeding, fluid and electrolyte problems, arrhythmias, reperfusion injury, airway complications, GI complications, pulmonary infarction, acute rejection,

Long term: Bleeding, fluid and electrolyte problems, arrhythmias, reperfusion injury, airway complications, GI complications, pulmonary infarction, acute rejection,

Main cause of mortality and morbidity: infections

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18
Q

Combined heart and lung transplant

A

Indications: Congenital heart disease (eg. eisenmernger’s syndrome- no. 1 indication), idiopathic PAH, and CF patients

Complications: HTN, renal dysfunction, hyperlipidaemia, diabetes, bronchiolitis obliterans, and coronary artery vasculopathy

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19
Q

AKI definition

A

A rapid deterioration in renal function over hours or days resulting in a sudden decrease in GFR. Can lead to dysregulation of fluid balance, acid-base homeostasis and electrolytes.

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20
Q

AKI complications

A

Hyperkalaemia, Hypo/hypernatraemia, Hypercalcaemia, Metabolic acidosis, Pulmonary oedema, Hypertension, Uraemic encephalopathy, Uraemic pericarditis

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21
Q

AKI risk factors

A
  • Chronic kidney disease
  • Heart failure
  • Liver disease
  • Diabetes
  • History of an AKI
  • Oliguria <0.5ml/kg/hr
  • Neurological or cognitive impairment, Hypovolaemia
  • Medication, iodine contrast
  • Age, deteriorating NEWS
22
Q

Stage 1 AKI

A
  • A rise of serum creatinine of 26umol/l or greater in 48 hours
  • A 50% or greater rise in serum creatinine in 7 days
  • Urine output <0.5ml/kg/hr for >6hr
23
Q

Stage 2 AKI

A
  • 100-200% rise of creatinine from baseline. OR
  • Urine output <0.5ml/kg/hr for >12 hours
24
Q

Stage 3 AKI

A
  • > 300% rise of creatinine from baseline. OR
  • Creatinine >350mol/L. OR
  • Urine output <0.3ml/kg/hr for 12hr or anuric for 12hr. OR
  • Requires Renal replacement therapy
25
Q

Management in stage 1 AKI

A
  • Optimise fluid status
  • Accurate fluid balance
  • Review medications, avoid nephrotoxic meds
  • Treat infection
  • Relieve obstruction
  • Inform senior team members
  • Monitor + act on NEWS
26
Q

Management in stage 2 and 3 AKI

A
  • Stage 2: senior review, consider catheterisation, consider renal referrral
  • Stage 3: senior review, 12 hourly bloods, Consider ITU referral, refer or discuss with renal
27
Q

Assessment of an AKI

A
  • Fluid status: pulse, blood pressure, peripheral perfusion, jugular venous pressure, peripheral oedema, weight
  • Renal function: serum electrolytes, urea and creatinine, urine output
  • Potential underlying causes
  • Look for other signs of renal damage: urine dipstick (blood, protein, signs of infection), urine microscopy (look for casts- look for inflammation and intrinsic causes)
  • Assess stage of AKI
28
Q

Causes of an AKI

A
  • Pre-renal is causes by transient renal hypoperfusion, usually reversible. Most common cause: normally have to give fluid, blood
  • Intrinsic due to structural damage to the kidneys
  • Post-renal is due to obstruction of the urinary tract, least common
29
Q

AKI risk factors

A
  • Dehydration
  • Age
  • Female
  • Back race
  • CKD
  • chronic disease (heart, lung, liver)
  • Diabetes mellitus, cancer, anaemia
30
Q

Pre-renal and post renal causes of an AKI

A
  • Hypovolaemia causes decreases cardiac output and effective circulating volume: heart failure, liver failure
  • Absolute hypovolaemia: haemorrhage, vomiting
  • Impaired renal autoregulation: NSAID’s, ARB’s, ACEi, cyclosporin
  • Systemic vasodilation: sepsis
  • Post-renal: Bilateral ureteropelvic obstruction, bladder outlet obstruction
31
Q

Intrinsic causes of an AKI

A
  • Acute glomerulonephritis: involves inflammation and damage to the glomerular membrane. Can have nephrotic and nephritic syndromes
  • Acute interstitial nephritis: an allergic reaction, caused by a variety of drugs
  • Acute tubular necrosis: caused by nephrotoxic agents and prolonged renal hypoperfusion causes ischaemic injury to the cells of the PCT
  • Inter-tubular obstruction: multiple myeloma with paraprotein pigment i.e. rhabdomyolysis
32
Q

Complications of an AKI 1

A
  • Hyperkalaemia: usually asymptomatic until severe, but can then cause muscle weakness, paralysis, cardiac arrhythmias, or (in extreme cases) cardiac arrest.
  • Other electrolyte imbalances= hyperphosphataemia, hyponatraemia, hypermagnesaemia, hypocalcaemia
  • Metabolic acidosis: Can present with altered level of consciousness, circulatory collapse, and hyperventilation. Low Bicarb
33
Q

Complications of an AKI 2

A
  • Volume overload (peripheral and pulmonary oedema)= Signs include tachypnoea, tachycardia, cyanosis, and lung crepitations. Often this is caused by excessive intravenous fluids being given to people in hospital who are anuric or oliguric.
  • Uraemia: occurs in severe AKI, requires dialysis. Symptoms include confusion, lethargy and altered levels of consciousness
  • CKD and end stage renal disease
34
Q

Predictors for CKD after AKI and AKI screen

A

Predictors for CKD after AKI: older age, low baseline eGFR, higher baseline albuminuria, higher stages of AKI

AKI screen
- Urine: dip, microscopy
- Bloods
- Renal ultrasound
- Renal biopsy: if no cause can be found

35
Q

AKI bloods

A
  • General: U&Es, Bone, LFTs, HB, Coag, creatinine kinase
  • Myeloma screen: Blood film, LDH, serum free light chains, serum electrophoresis, Ig, urine Bence Jones proteins
  • Vasculitis: ANCA ( MPO-PR3), Anti-GBM
  • Autoimmune: Complement, Immunoglobulins, Rheumatoid factor, Antiphospholipid antibody
  • Infection: Hep B, C, HIV, ASOT
  • Malignancy: PSA
36
Q

Treatment for end stage kidney disease

A
  • Haemodialysis: uses a filtering machine to remove waste and extra fluid from your blood. Performed at hospital 3 times a wee
  • Peritoneal dialysis: done through the lining in the abdomen, fluid is put in the abdomen and filtered across. Can be done at home
  • Kidney transplant: must be fit enough to undergo surgery and immunosuppressant
  • Conservative: if don’t want dialysis is about improving QoL and reducing symptoms
37
Q

Causes of pre-renal AKI

A
  • Sepsis: blood pressure falls due to vasodilation
  • Volume, diarrhoea, severe bleeding: volume depletion
  • Dehydration
  • Reduced cardiac output or heart failure causing hypotension
38
Q

Post renal causes of an AKI

A
  • Males with benign prostatic hyperplasia (BPH), prostate cancer
  • Females - Pelvic/abdominal masses
  • Kidney/renal tract stones, malignancy, strictures
  • Ureters: nephrolithiasis, retroperitoneal fibrosis
  • Urethra: urethral strictures
  • Congenital obstructive uropathy presenting in neonates (especially males with posterior urethral valves).
  • Obstruction at or distal to the bladder causes an AKI in both kidneys
39
Q

Intrinsic causes of an AKI

A
  • Prolonged ‘pre-renal’ AKI, whereby a sustained drop in blood pressure results in cell damage (most common cause)
  • Medications that may exacerbate hypovolaemia and hypotension: ACEi, ARB’s, loop diuretics
  • Toxins; contrast, myoglobin (released during muscle injury), glomerulonephritis, tubulointerstitial nephritis
  • Vasculitis, myeloma
40
Q

Intrinsic causes of an AKI and what part of the nephron it affects

A
  • Glomerulus (glomerulonephritis): vasculitis, Goodpasture’s, SLE, Immunoglobulin A nephropathy
  • Tubule obstruction: myeloma casts, urate crystals, pigment casts secondary to rhabdomyolysis.
  • Tubular injury: Myeloma, acute tubular necrosis (most common), Aminoglycosides, Rhabdomyelosis When there is damage to the renal parenchyma causing scarring and fibrosis
  • Interstitum: Pyelonephritis, medication (NSAID’s), infiltration by malignancy or sarcoidosis
  • Vessels: vasculitis, accelerated hypertension, Haemolytic-uraemic syndrome (HUS), Thrombotic thrombocytopenic purpura (TTP)
41
Q

Management of AKI

A
  • ABCDE assessment
  • Assessment of fluid status: JVP (most reliable in right sided heart failure), presence of peripheral oedema, Mucous membrane/skin turgor, fluid input/output chart, pulse and blood pressure, change in weight
  • Fluid resuscitation and maintenance of euvolemia
  • Regular bloods (creatinine, urea and electrolytes)
  • Fluid balance chart
42
Q

Post renal causes of an AKI in different parts of the urinary system

A
  • Ureters: Luminal (ureteric calculi, vesicoureteric reflux), Mural (tumour), Extrinsic (compression from abdominal/pelvic mass, retroperitoneal fibrosis)
  • Bladder: Luminal (bladder calculi), Mural (tumour i.e. bladder carcinoma), Extrinsic (neurogenic bladder, diabetes mellitus, MS, Spinal cord compression)
  • Urethra: Luminal (blocked urethral catheter), Mural (urethral stricture), Extrinsic (BPH, Prostatic carcinoma, Pain)
43
Q

Clinical findings of an AKI

A
  • Oliguria or anuria
  • Signs of hypovolaemia: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
  • Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
  • Signs of uraemia: ecchymosis due to platelet dysfunction, uraemic encephalopathy (e.g. asterixis, confusion, seizures)
  • Signs of post-renal obstruction: palpable or tender distended bladder
44
Q

AKI: bedside investigations

A
  • Urine dipstick
  • Urine microscopy
  • Urine osmolality and electrolytes
  • Fluid status chart: use catheter to measure urine volume
  • ECG
45
Q

AKI investigations bloods

A
  • FBC, U&E, LFT, bone profile
  • Blood gas (venous/arterial)
  • To look for cause: CK, vasculitis screen (ANCA, ANA), clotting, blood film, complement, Immunoglobulins, Serum electrophoresis, virology (hepatitis B/C)
46
Q

AKI imaging

A
  • CXR (look for signs of overload)
  • Renal doppler (renal vascular assessment)
  • Kidney and bladder ultrasound: looks for obstruction i.e. hydronephrosis
  • Magnetic resonance angiography (renal vascular assessment)
  • CT non-contrast: radiopaque and non-radiopaque calculi, ureteric obstruction
  • CT urogram: investigate for urinary tract bleeding
  • Renal biopsy: intra-renal AKI or rapidly progressive
47
Q

AKI general management

A
  • Withdraw nephrotoxic medication
  • Fluid resuscitation in hypovolaemia/hypotension
  • Catheterisation: relieves urinary obstruction
  • Assess for sepsis and initiate sepsis 6
  • Monitor fluid balance with input/output charts and daily weight
  • Daily U&E’s, urine osmolality and sodium
  • Urinalysis +/- culture, urinary PCR or nephritic screen
48
Q

ABCDE checklist for AKI management

A
  • A: address drugs
  • B: boost blood pressure
  • C: calculate fluid balance
  • D: dip urine
  • E: exclude obstruction
49
Q

Targeted management of AKI- depends on underlying cause:

A
  • Diuretics may benefit volume overloaded patients, particularly in
    pulmonary oedema
  • Immunosuppression with glucocorticoids can be considered in
    AIN or RPGN to slow the progression to irreversible injury7
  • Some patients may need an indwelling bladder catheter,
    nephrostomy tubes or ureteric stent insertion depending on the
    site and cause of the obstruction
50
Q

When is RRT indicated

A
  • Metabolic acidosis pH < 7.15 or worsening acidaemia
  • Refractory electrolyte abnormalities (hyperkalaemia >6.5mmol) or rapidly rising K+ levels
  • Presence of dialysable toxins (toxic alcohols, aspirin, lithium)
  • Refractory fluid overload (diuretic resistant fluid overload in
    setting of AKI)
  • End-organ uraemic complications (e.g. pericarditis,
    encephalopathy, uraemic bleeding)
  • Urine output <0.3ml/kg for 24 hours, absolute anuria for >12 hours
  • Multi-organ failure, severe hypo/hyperthermia