SAMPLES FOR THE SPECIALITY CERTIFICATE EXAMINATIONBy:Dr Nihal AbosaifConsultant Acute Physician

QUESTION: 1A 40-year-old woman with known alcoholic liver disease

admitted with upper gastrointestinal bleeding. She required 2 units of blood transfusion before having oesophageal banding of her varices. She became oliguric two days after admission with worsening GFR.

 Investigations:

haemoglobin 90 g/L (115-165)serum sodium 135 mmol/L(137-144)serum urea 25 mmol/L(2.5-7)serum creatinine 280 µmol/L(60-110)eGFR 24mL/min(>60)serum albumin 26 g/L(37-49)urine sodium 50 mmol(15-250)urine osmolality 287 mosmol/kg(350-1000)urine creatinine 5 mmol(9-18)

WHAT IS THE MOST LIKELY DIAGNOSIS?

A. acute interstitial nephritisB. acute tubular necrosisC. glomerulonephritisD. hepatorenal syndromeE. prerenal azotaemia

Answer key: B

60-70% 20% 10%

RIFLE CLASSIFICATION

ACUTE KIDNEY INJURY NETWORK - DIAGNOSTIC CRITERIA FOR ACUTE KIDNEY INJURY (AKI)

An abrupt (within 48 hours) reduction in kidney function defined as

an absolute increase in serum creatinine of more than or equal to ≥ 26.4 μmol/l (0.3 mg/dl), or

a percentage increase in serum creatinine of ≥ 50% (1.5-fold from baseline),

or a reduction in urine output of ≤ 0.5 ml/kg per hour for > six hours.

Mehta et al, Critical Care Med 2007; 11: R31

ACUTE KIDNEY INJURY NETWORK – STAGING SYSTEM FOR AKI

Stage Serum creatinine criteria Urine output criteria

1 Increase in serum creatinine by (≥26.2 µmol/L) OrIncrease ≥ 150-200% from baseline

Urine output < 0.5ml/kg/hr > 6 hr

2 Increase in serum creatinine > 200-300% from baseline

Urine output < 0.5ml/kg/hr > 12 hr

3 Increase in serum creatinine > 300% from baselineOrSerum creatinine ≥354µmol/L with an acute rise of > 44.2 µmol/LOrTreatment with renal replacement therapy

Urine output < 0.3ml/kg/hr x 24 hr OrAnuria x 12 hr

Mehta et al, Critical Care Med 2007; 11: R31

LONG TERM OUTCOME OF AKI 206 ICU patients with AKI were

randomized in a trial comparing haemofiltration versus haemodiafiltration.

Of these, 95 (46%) survived at 90 days. Post-discharge information relating to 3-

year survival and renal function was successfully obtained in 89 (94%) of the patients.

Of the 89 patients studied, chronic kidney disease (CKD) was present in 32 subjects from the onset, and CKD developed de novo in 25 patients following AKI.

End-stage renal disease (ESRD) developed in 9 patients (of whom 8 had pre-existing CKD) and 29 patients died.

Three-year survival was 67% overall; the mortality at 3 years was 50% for those with pre-existing kidney disease, and 71 and 82% for those with de novo and without CKD, respectively.

Triverio et al Nephrol Dial Transplant 2009; 24 (7): 2186-89

Kaplan–Meyer analysis of 3-year survival rates in patients without (no CKD prior to AKI) and with prior (prior CKD to AKI) or de novo CKD after AKI.

AKI stage 1Treat underlying problems (dehydration, sepsis etc.)Treat acute complications (acidosis, hyperkalaemia, respiratory failure)-Consider renal screen (ANCA, Anti GBM Ab, Immunoglobulins & paraprotein, urine BJP)

-If no improvement: consider renal referral

AKI stage 3

Same as AKI stage 2- Refer renal

Confirmed AKI• Treat underlying problems (dehydration, sepsis etc.)• Treat acute complications (e.g. acidosis, hyperkalaemia,

respiratory failure)• Urine dip test and microscopy• Stop any nephrotoxic drugs e.g.NSAID. Avoid gentamicin /

contrast• Withhold anti-hypertensives if hypotensive• Urinary catheter and strict fluid balance monitoring• Daily U & Es• Urgent renal ultrasound scan • Urgent senior review

Diagnosis of AKI

AKI stage 2

Treat underlying problems-Treat acute complications (acidosis, hyperkalaemia, respiratory failure)- Urgent renal screen- Refer renal

Proposed Acute Kidney Injury (AKI) Guideline

QUESTION: 2

A 30-year-old man with bipolar disorder presented with confusion and dehydration. He has been treated with lithium for the past 10 years.

On examination, His GCS was 10/15 with no focal neurological signs. A CT-head was normal.

 

Investigations:

haemoglobin 146 g/L (115–165)

platelet count 254 109/L (150–400)

serum sodium 165 mmol/L (137–144)

serum potassium 4.4 mmol/L (3.5–4.9)

serum creatinine 170 µmol/L (60–110)

serum urea 20 mmol/L (2.5-7.0)

serum bicarbonate 12 mmol/L (21-29)

urine osmolality 80 mosmol/kg (350-1000)

 

urinalysis normal

 

WHAT IS THE MOST LIKELY DIAGNOSIS? 

A. chronic hyperventilationB. excessive solute intakeC. diabetes insipidusD. gastrointestinal lossesE. excessive use of diuretics

Answer key: C

WHAT DO YOU THINK THE TREATMENT SHOULD BE?

A. intravenous normal salineB. intravenous half normal salineC. intranasal desmopressinD. intravenous dextrose 5% solutionE. diuretics

Answer Key: B or D

TYPES OF DIABETES INSIPIDUS Central diabetes insipidus is caused by the inability to secrete

(and usually to synthesize) vasopressin in response to increased osmolality.

Nephrogenic diabetes insipidus is caused by the inability of an otherwise normal kidney to respond to vasopressin. Unlike central diabetes insipidus, however, measured levels of vasopressin in plasma are high or appropriate for plasma osmolality.   

Gestational diabetes insipidus is a rare condition produced by elevated levels or activity of placental cystine aminopeptidase (oxytocinase or vasopressinase) during pregnancy. Because of the circulating vasopressinase, plasma vasopressin levels usually cannot be measured.   

Primary polydipsia is a disorder of thirst stimulation rather than of vasopressin secretion or activity. Excessive ingested water produces a mild decrease in plasma osmolality that shuts off secretion of vasopressin. The amount of vasopressin in plasma is unmeasurable or low but is but is appropriate for the low plasma osmolality.

QUESTION: 3

A 34-year-old man brought to emergency department with confusion. He had a history of alcohol dependence. He was somnolent and did not answer questions.

On examination, Blood pressure 130/80 mmhg, heart rate 120/minute, respiratory rate 24/minute and temperature 37◦C. The rest of examination was unremarkable.

 Investigations:

microscopic urinalysis calcium oxalate crystals. Which of the following most likely will be found on further investigations?

A. more than 10.000 bacterial colonies on urine culture

B. anion gap metabolic acidosis

C. hydronephrosis on ultrasound

D. nephrolithiasis on CT scan

E. positive antinuclear antibodies (ANA)

 

Answer key: B

CALCIUM OXALATE CRYSTALS IN ETHYLENE GLYCOL TOXICITY

Accumulation of COM crystals in the kidney is responsible for producing the renal toxicity associated with EG poisoning.

The development of a pharmacological approach to reduce COM crystal adherence to tubular cells and its cellular interactions would be valuable as this would decrease the renal toxicity not only in late treated cases of EG poisoning, but also in other hyperoxaluric diseases such as primary hyperoxaluria and kidney stone formation.

SYSTEMIC SCLEROSIS/SCLERODERMAQUESTION: 4

A 50-year-old woman with a diagnosis of diffuse cutaneous scleroderma was admitted with malignant hypertension, oliguria, oedema, haemolytic anaemia and renal failure. You diagnosed the patient with scleroderma renal crisis.

  What is the best recommended treatment? A. enalaprilB. atenololC. amlodipineD. glyceril trinitrateE. nitroprusside

Answer key: A

DIAGNOSIS AND TREATMENTQUESTION 5A 70-year-old woman admitted with upper abdominal pain, weight

loss and constipation. She was also tachypoenic, tachycardic and distressed. She used to be a heavy smoker for more than 40 years.

On examination, blood pressure 160/90, heart rate 130/minute, respiratory rate 30/minute and O2 saturation was 95% on 10 litres of O2. Her jugular venous pressure was raised, chest auscultation revealed bilateral basal crepetations, normal heart sounds with functional systolic murmur.

 Investigations:

haemoglobin 80 g/L (115–165)platelet count 250 109/L (150–400)

 serum sodium 143 mmol/L (137–144)serum potassium 6.5 mmol/L (3.5–4.9)serum creatinine 490 µmol/L (60–110)serum calcium 3.8 mmol/L (2.2-2.6)

WHAT IS THE MOST APPROPRIATE NEXT STEP IN MANAGEMENT?

A.  intravenous normal salineB. intravenous frusemideC. blood transfusionD. haemodialysisE. intravenous calcium gluconate

Answer key: D

QUESTION: 6

An 83-year-old woman presented with two-month history of increasing leg swelling. She also lost 10 kilograms of her weight. No other signs of heart failure. Despite the commencement on 80 mg of furosemide, she became more oedematous and breathless.

 On examination, she looked pale, malnourished and has generalised

anasarca. Investigations:

haemoglobin 90 g/L (115–165)platelet count 80 109/L (150–400)

 serum sodium 126 mmol/L (137–144)serum potassium 4.4 mmol/L (3.5–4.9)serum creatinine 100 µmol/L (60–110)

 urinalysis 4+ protein, 1+ blood

WHAT IS THE NEXT APPROPRIATE INVESTIGATION?

A.  abdominal ultrasoundB. upper endoscopyC. urine protein creatinine ratio (PCR)D. Whole body CTE. chest X ray

Answer Key : D

Her autoimmune profile was normal, anti neutrophil cytoplasmic antibody (ANCA) was normal. Negative Anti GBM antibody. CT abdomen showed enlarged lymph nodes in the para-aortic, inguinal and omental infiltration. Renal biopsy showed minimal change disease. Despite the commencement on 80 mg of furosemide, 60 mg of steroids for two month, she became more oedematous and breathless.

Investigations: haemoglobin 90 g/L (115–165)platelet count 80 109/L (150–400)

 serum sodium 126 mmol/L (137–144)serum potassium 4.4 mmol/L (3.5–4.9)serum creatinine 100 µmol/L (60–110)serum cholesterol12mmol/L (3.5-5.0)urine protein creatinine ratio 2000mg/mmol (<15)

QUESTION: 7

WHAT IS THE MOST LIKELY DIAGNOSIS?

A.  unresponsiveness to treatmentB. thromboembolic diseaseC. focal segmental glomerulosclerosisD. underlying malignancyE. renal vein thrombosis

Answer key: E

QUESTION 8:

A 29-year-old man admitted with an episode of severe asthma. He was given nebulised β-adrenergic agonists and steroids. He did not respond well to this treatment and became more exhausted with development of type 2 respiratory failure. He was commenced on bi-level positive airway pressure ventilation. After 18 hours of this treatment, he began to improve but started to complain of fatigue, myalgia and leg weakness. .

 On examination, he has 3 out of 5 motor weakness in

both legs. No other positive neurological findings. Investigations: Electrocardiography shows flat T-waves, ST-depression

and prolonged QT interval.

WHAT IS THE MOST LIKELY CAUSE OF HIS SYMPTOMS AND FINDINGS?

A.  adrenal insufficiencyB. myocardial infarction with congestive heart

failureC. medication effectD. Todd’s paralysisE. psychological paralysis

Answer key: C

QUESTION 9:

An 80-year-old man with a history of diabetes mellitus was found to have a lung nodule on his chest-X-Ray. He was suspected to have lung cancer. A CT-chest with contrast was performed to confirm the diagnosis. Two weeks later, he developed shortness of breath, bilateral lower limb oedema, maculopapular skin rash on the shin of tibia and oliguria.

 Investigations:

haemoglobin 104 g/L (115–165)platelet count 364 109/L (150–400)

 serum sodium 145 mmol/L (137–144)serum potassium 6.0 mmol/L (3.5–4.9)serum creatinine 300 µmol/L (60–110)

 urine protein creatinine ratio 200mg/mmol (<15)urine microscopy >200 white cells

>100 red blood cells

URINE MICROSCOPY

WHAT IS THE MOST LIKELY DIAGNOSIS? 

A. Acute tubular necrosisB. Allergic hypersensitivityC. Immune complex glomerulonephritisD. Cholesterol emboliE. Prerenal azotaemia

Answer key: D

CONTRAST NEPHROPATHY

Contrast induced nephropathy (CIN) is the third leading cause of hospital acquired renal failure and is associated with significant morbidity and mortality. Chronic kidney disease is the primary predisposing factor for CIN. As estimated glomerular filtration rate <60 ml/1.73 m2 represents significant renal dysfunction and defines patients at high risk.

Mechanism of contrast inducted Nephropathy

STRATEGIES FOR PREVENTING CONTRAST-INDUCED NEPHROPATHYStrategies that do not work

Mannitol Furosemide Dopamine Atrial natriuretic factor Fenoldopam Haemodialysis

Strategies that may work Calcium channel blockers Theophylline Iso-osmolar contrast media N-acetylcysteine Hemofiltration Sodium bicarbonate Ascorbic acid Prostaglandins

Currently recommended strategies Employ noniodinated contrast studies Avoid nonsteroidal anti-inflammatory drugs Provide adequate time between contrast procedures Minimize contrast volume Parenteral hydration Low-osmolar or iso-osmolar contrast media

KEY POINTS The risk of contrast-induced nephropathy is directly proportional to

the severity of pre-existing renal insufficiency. Hydration with normal saline solution is the most widely accepted

preventive intervention. N-acetylcysteine may be effective, but studies have given

conflicting results. Sodium bicarbonate may be of value, but larger multicenter

studies are needed to determine its true effectiveness. Newer contrast agents that are nonionic and of lower osmolality

than older agents are less nephrotoxic but can still cause nephropathy.

Due to the logistical effort and high cost associated with hemofiltration, larger randomized trials should be performed before this technique can be recommended as standard prophylaxis against contrast-induced nephropathy in high-risk patients.

Theophylline cannot yet be recommended as standard prophylaxis against contrast-induced nephropathy.

QUESTION 10:

A 50-year-old woman with known end stage renal failure who is having haemodialysis through a tunnelled catheter in the Rt. internal jugular vein presented with fever, rigors and hypotension. She also suffered from severe lower back pain.

On examination, her blood pressure was 90/50, heart rate 150/minute, respiratory rate 25 per minute, temperature 38.5 c. She was sweaty, restless and skin examination at the site of line exit was red, tender and warm. Cardiac examination showed normal heart sounds with a mid systolic apical murmur which was new.

 Investigations:

  haemoglobin 90 g/L (115–165)

platelet count 164 109/L (150–400)

white blood cells 25 X109/L (40-100)

neutrophils 23X109/L ()

 

serum sodium 143 mmol/L (137–144)

serum potassium 4.4 mmol/L (3.5–4.9)

serum creatinine 650 µmol/L (60–110)

serum alkaline phosphatase 400 U/L(45-105)

WHAT IS THE MOST LIKELY DIAGNOSIS?

A. line sepsisB. infective endocarditisC. discitisD. exit site infectionE. Septicaemia

Answer Key A

What is most likely cause of back pain in this patient:

A. Compression fracture of the spineB. discitisC. infective endocarditisD. Multiple myelomaE. Vertebral metastasis

Answer Key: B

Any Questions