WEEK 8 - an acutely unwell patient Flashcards

Question

in patients with sepsis, what is initial fluid resuscitation with?

Answer 1

a crystalloid given as a bolus over less than 15 minutes eg. 500mL of 0.9% sodium chloride 500 mL of Hartmann’s solution over 10 minutes

Answer 2

crystalloids and colloids

Answer 3

Crystalloids are solutions containing small molecules in water (e.g. sodium chloride, glucose, Hartmann’s) Colloids are solutions with large molecular weight substances (e.g. albumin, gelatins)

Answer 4

Lactate is raised as a result of tissue hypoxia in sepsis; as a result of widespread systemic inflammation, there is organ hypoperfusion and subsequently the cells turn to anaerobic metabolism, which produce lactate. A raised lactate of > 4.0mmol/L is considered a high risk criteria for sepsis (these patients are at high risk of deterioration)

Answer 5

tall, tented T waves, and broad QRS complexes (>0.12ms), with no discernible P waves These are all ECG changes seen in hyperkalaemia

Answer 6

Hyperkalaemia can be due to several causes: - Reduced renal excretion of potassium - Increased circulating serum potassium – this can be exogenous (from potassium supplementation) or endogenous (tumour lysis syndrome, rhabdomyolysis, burns) - Pseudohyperkalaemia – where there isn’t a true elevation in serum potassium; suspect this and repeat bloods as soon as possible for serum potassium in patients with isolated, unexpected blood results of hyperkalaemia who are well and have no ECG signs, as it may be due to test tube haemolysis or prolonged torniquet time Of those listed, it is most often due to acute renal failure and medications (e.g. ACE-inhibitors) in hospitalised patients.

Answer 7

- 6.5 - ECG

Answer 8

1. Protecting the cardiac membrane – IV calcium gluconate acts by reducing membrane excitatory effects of K on cardiac tissue rapidly, therefore reducing the potential for cardiac arrhythmias such as ventricular fibrillation, but has minimal effect on lowering serum K concentrations. 2. Shifting potassium intracellularly – give 10 units Insulin with 25g glucose (an example of a treatment regime for this would be 10 units Actrapid in 250mls of 10% dextrose at 50ml/hr for 5 hours (25g)). You will see in some guidelines the recommendation of 50ml 50% Dextrose over 15minutes however this requires a central line and risks extravasation and tissue damage if used peripherally. This regime is generally avoided in clinical practise and it should only be used after senior advise if there are concerns about the volume of fluid you are giving patients who are fluid overloaded. Nebulised salbutamol 10 – 20mg is also given alongside insulin and glucose in severe, life-threatening hyperkalaemia (Avoid salbutamol if tachyarrhythmia present) 3. Stopping any contributing medications – such as ACE-inhibitors, potassium-sparing diuretics.

Answer 9

- sodium zirconium cyclosilicate and patiromer - promoting potassium excretion

Answer 10

1. filter and excrete nitrogenous waste products 2. Maintain acid-base balance, by controlling reabsorption and excretion of electrolytes (e.g., sodium, potassium, chloride, etc.) 3. Produce certain hormones (erythropoietin, renin, calcitriol)

Answer 11

creatinine

Answer 12

1/creatinine

Answer 13

1. increasing re absorption of sodium ions 2. vasoconstriction the efferent arterioles

Answer 14

- 25% - hypovolaemia - ACE-inhibitors and NSAIDs - RAAS

Answer 15

This condition is usually the result of a combination of factors which have caused renal ischaemia and toxicity, e.g., hypotension and dehydration or sepsis with associated nephrotoxic drugs. The histology of ATN does not usually show frankly necrotic cells, but sloughing of the renal tubular epithelium causing dilation and obstruction of tubules and some mild leukocyte infiltration. Treatment is supportive, there are no specific drug treatments, and withdrawal of nephrotoxic agents or treatment of associated sepsis. Usually there is recovery after 2-3 weeks (maximum 6 weeks). There is a high mortality associated with ATN (approx 50%), but this is usually because of the associated illnesses (e.g., septic shock), age, etc. Once recovered only a very small proportion of people are left with chronic kidney disease. The severity of this illness is the reason such effort is made to recognise risk factors and prevent this disease.

Answer 16

1. oligouric phase 2. maintenance phase 3. polyuric recovery phase

Answer 17

= oligouric phase the kidneys produce less than 500mls of urine per day. patients in this phase are vulnerable to fluid overload and electrolyte imbalance esp K+. creatinine levels usually rise quite rapidly during this phase

Answer 18

= maintenance phase the patient is no longer oligouric and this increased urinary output helps maintain fluid and electrolyte balance. creatinine levels are usually stable or rise very slowly

Answer 19

= polyuric recovery phase In this phase the kidneys produce large quantities of dilute urine, so large in fact patients can become hypovolaemic and unwell. There are a number of causes for this phase postulated, but one explanation is that the distal tubules and collecting ducts recover last and in particular their aquaporin channels. These damaged aquaporin channels do not allow water to be reabsorbed and therefore high quantities of dilute urine are produced. Patients are also susceptible to electrolyte loss (e.g. hypokalemia) in this phase. Creatinine levels falls swiftly in this phase.

Answer 20

The loss of the kidneys’ homeostatic functions in AKI will mean that the kidneys are: 1. Unable to regulate acid-base balance, leading to hyperkalaemia, fluid retention and metabolic acidosis 2. Unable to excrete metabolic waste products, leading to build-up of urea and creatinine Eventually, this may lead to multi-organ failure.

Answer 21

sepsis can be a cause of disseminated intravascular coagulation (DIC)

Answer 22

disseminated intravascular coagulation - a clinical syndrome characterised by dysregulated coagulation - several causes inc: sepsis, trauma, malignancy, obstetric complications (eg amniotic fluid embolism, placental abruption) - in these conditions, tissue factor (TF) is released into the bloodstream as a result of cytokine release, endotoxin release or endothelial damage, which activates the coagulation pathway - this widespread coagulation consumes clotting factors, which causes bleeding in addition to micro vascular thrombosis - management involves treating the underlying cause, and supportive blood product (platelet or FFP) transfusions in life-threatening bleeding, severe thrombocytopenia or when patients need to undergo urgent invasive interventions without delay.

Answer 23

1. pre-renal (85%) — reduced perfusion of the kidneys, either from hypovolaemia, reduced renal blood flow or reduced cardiac output, which leads to reduced glomerular filtration rate (GFR) 2. renal (intrinsic) — structural damage to the glomeruli, interstitial, and/or tubules 3. post-renal AKI — acute obstruction of urinary flow, which increases intra-tubular pressures and subsequently decreases GFR

Answer 24

Age 65 years or over; History of AKI; CKD (eGFR < 60mL/min/1.73m2); Symptoms or history of urological obstruction, or conditions which may lead to obstruction; Chronic conditions such as heart failure, liver disease, diabetes mellitus; Neurological or cognitive impairment or disability (which may limit fluid intake because of reliance on a carer); Sepsis; Hypovolaemia; Oliguria (urine output < 0.5 mL/kg/h); Nephrotoxic drug use within the last week; Exposure to iodinated contrast agents within the past week

Answer 25

history: poor oral intake or dehydration, diarrhoea or vomiting examination: signs of sepsis, assessment of volume status - HR, cap refill, BP, JVP, poor skin turgor, signs of renovascular disease - abdominal bruits, impalpable peripheral pulses

Answer 26

history : Constitutional symptoms – fever, rash, joint pains, nasal crusting, weight loss; History of fall with long lie (may cause rhabdomyolysis); Use of OTC medications such as NSAIDs; Use of nephrotoxic medications examination : rash, uveitis, joint swelling

Answer 27

history : Lower Urinary Tract Symptoms (LUTS) in men – urinary frequency, urgency – may be secondary to enlarged prostate; History of renal calculi – may cause hydronephrosis and obstruction examination : abdo exam - palpable bladder

Answer 28

- urine dipstick - urine output

Answer 29

glomerulonephritis

Answer 30

if any of the following features are present AND they are refractory to medical therapy: 1. Hyperkalaemia 2. Pulmonary oedema 3. Severe metabolic acidosis 4. Uraemia – uraemic pericarditis or encephalopathy 5. Ingestion of certain toxins

Answer 31

- accumulate - hypoglycaemia

Answer 32

oxycodone, fentanyl and hydromorphone

Answer 33

Furosemide may actually improve renal function in patients who have AKI secondary to cardiorenal syndrome. In these patients, the heart fails to pump adequately, leading to reduced cardiac output and systemic hypotension. The renin-angiotensin system is activated, which causes renal efferent arteriolar vasoconstriction and inadequate glomerular perfusion. If furosemide is given to achieve diuresis in someone with fluid overload, this decreases ventricular filling pressures and improves their symptoms. The glomerular filtration will eventually improve as there will be more blood flow through the kidneys from improved cardiac output and efferent arteriolar vasodilatation. However, you may notice that there is initially a worsening of their AKI, as creatinine levels are diluted in fluid overload; removal of the excess fluid unmasks their true kidney function. In certain circumstances of AKI you may withhold a loop diuretic.

Answer 34

acute interstitial nephritis Many medications can cause acute interstitial nephritis (AIN). This is a clinical syndrome characterised by inflammatory infiltrates in the renal interstitium (seen on renal biopsy), in response to a drug, infection or autoimmune process. Patients rapidly develop an AKI within 2 weeks of starting the medication, and can either be asymptomatic, or present with constitutional symptoms (rash, malaise, fever). Some examples of medications which can rarely cause AIN include proton pump inhibitors, penicillins, NSAIDs, allopurinol, aciclovir.

Answer 35

pus in the renal pelvis characterized by the accumulation of purulent debris and sediment in the renal pelvis and urinary collecting system

Answer 36

- refractory metabolic acidosis - refractory pulmonary oedema - refractory hyperkalaemia - uraemia encephalopathy

Answer 37

5 - age - diabetes - NSAID use - hypertension - history of AKI

Answer 38

heart rate / BP

Answer 39

‘how fast you fill the pump and squeeze’: - The ‘fast’ is the heart rate - The ‘fill’ is the blood volume - The ‘pump’ is the heart - The ‘squeeze’ is the blood pressure

Answer 40

Shock is a descriptive term used to describe the state that results when circulatory insufficiency leads to inadequate tissue perfusion and thus inadequate oxygen delivery to tissues. This shortage of oxygen means that aerobic metabolism cannot occur, resulting in organ dysfunction

Answer 41

- altered mental state - mottled and clammy skin - oliguria - elevated blood lactate - tachycardia

Answer 42

- Hypovolaemic (e.g., haemorrhagic, dehydration) - Distributive (e.g., sepsis, anaphylaxis) - Obstructive (e.g., pulmonary embolism, tension pneumothorax) - Cardiogenic (e.g., myocardial infarction) - Neurogenic (e.g., cervical spinal cord injury)

Answer 43

- bleeding - loss - cool - good

Answer 44

- infection - febrile - hypotension

Answer 45

respiratory distress, asymmetric chest expansion, dilated neck veins, tracheal deviation away from affected side, absent breath sounds on affected side, hyperresonant percussion note on affected side

Answer 46

dilated neck veins, muffled heart sounds

Answer 47

- a specific syndrome that happens in trauma - different to spinal shock - happens in high (cervical or high thoracic) spinal cord injuries where the patient loses their sympathetic outflow, hence their normal sympathetic responses to blood loss: - instead of tachycardic, they will be bradycardic - and instead of hypotension and peripherally vasoconstricted/cold, they will be hypotensive but peripherally dilated/warm

Answer 48

a screening tool to assess the likelihood that a person with an acute upper GI bleed will need to have a medical intervention such as a blood transfusion or endoscopic intervention

Answer 49

assesses the risk of death in UGIB

Answer 50

- crystalloid and blood - 70g/L - 70-100g/L - PPI - terlipressin

Answer 51

Rhabdomyolysis is a syndrome whereby there is breakdown and necrosis of damaged skeletal muscle, releasing its contents (electrolytes, myoglobin, sarcoplasmic proteins such as creatinine kinase) into the circulation. It can cause multiple complications, including AKI as the myoglobin deposits in and obstructs the renal tubules.

Answer 52

IV plasmalyte 500mL over 10 mins this patient is dangerously dehydrated and showing sings of hypovolaemic shock. NICE guidance on IV fluids tells us that, for resuscitation, we should prescribe 250-500mL of a crystalloid IV STAT/over less than 15 mins

Answer 53

IM adrenaline 0.5mL 1:1000 The patient is shocked and the features of tongue swelling causing airway compromise and pallor suggesting severe illness/ hypotension, as well as features of an uritcarial rash and a possible food exposure in a restaurant, suggest that his shock is due to anaphylaxis. The treatment for this is IM adrenaline 500mcg or 0.5mL of 1:1000. We use 1:1000 IM because it is more concentrated, thus a smaller amount can be injected into the muscle. In cardiac arrest, we use 1:10000 IV because it is less concentrated so it is less likely to cause phlebitis.

Answer 54

ECG and prescribe IV calcium gluconate A potassium of 6.7 is dangerously high and so we should immediately review the patient, undertake an ECG, and protect the cardiac membrane with IV calcium. This will usually be 10mLs of 10% calcium gluconate IV over 10 minutes which is equivalent to 2.2mmol of calcium and can be repeated if the ECG has not improved). After these initial life-saving actions have been undertaken, it would be appropriate to prescribe IV insulin-dextrose (usually 5-10 units of fast acting insulin in 50mLs of 50% glucose over 5-10 minutes) and nebulised salbutamol to drive potassium out of the serum and into the cells.

Answer 55

raised anion gap metabolic acidosis due to elevated lactate The pH of 7.28 shows an acidosis. However, blood gases may show several synchronous processes so don’t forget to work out the anion gap to confirm or refute the presence of raised anion gap metabolic acidosis. In this case, the acidotic pH is likely due to the addition of unmeasured anions or lactate. This is commonly due to hypoperfusion such as caused by sepsis or other causes of shock, but it can also be due to medications such as metformin or salbutamol.

Answer 56

ramipril Ramipril (an ACE-inhibitor) has many long-term benefits for patients with certain chronic diseases. However, many patients with acute illness have hypotension, AKI, and hyperkalaemia. Ramipril has antihypertensive effects and it also reduces renal hyperfiltration which can reduce eGFR and increase potassium, all things we want to avoid in the acutely unwell patient. Hence, NICE advises us to temporarily suspend it in the setting of acute hypotension and AKI. Remember that many drugs are renally excreted. The patient’s apixaban and metformin prescriptions will need to be reviewed if the eGFR continues to drop.

Answer 57

(Na+ + K+) - (Cl- + HCO3-) = measure of acid-based balance If the anion gap is too high, your blood is more acidic than normal. If the anion gap is too low, your blood isn't acidic enough.

WEEK 8 - an acutely unwell patient Flashcards

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