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MRCOG PART 1 - CLINICAL MX & DATA

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MRCOG Part I single best answers: Peri-operative care

Answers Posted by Farrukh G.

 

*1) C

  • The normal sodium intake in adults is 50-100 mmol/24 hours, which should be accompanied by about 1.5 to 2.5 L (25 to 35 mL/kg/24h) of water
  • Chloride ions cause renal vasoconstriction and reduce glomerular filtration rate resulting in sodium retention
  • Because of the risk of inducing hyperchloraemic acidosis when crystalloid resuscitation or replacement is indicated, balanced salt solutions e.g. Ringer’s lactate/acetate or Hartmann’s solution should be used instead of 0.9% saline, except in cases of hypochloraemia e.g. from vomiting or gastric drainage.

 

*2) E

  • Solutions such as 4%/0.18% dextrose/saline and 5% dextrose are important sources of free water for maintenance, but should be used with caution as excessive amounts may cause dangerous hyponatraemia, especially in children and the elderly. These solutions are not appropriate for resuscitation or replacement therapy except in conditions of significant free water deficit e.g. diabetes insipidus.

*3) C

*4) D

*5) C

  • To meet maintenance requirements, adult patients should receive sodium 50-100 mmol/day, potassium 40-80 mmol/day in 1.5-2.5 litres of water by the oral, enteral or parenteral route. Additional amounts should only be given to correct deficit or continuing losses.

*6) = 3) = C

 

*7) = 4) = D

 

*8) = 5) = C

 

Apologies these questions were repeated

 

Type

Na (mM)

K (mM)

Cl (mM)

Osmolarity

(mosmol/L)

Plasma vol expansion duration (h)

Plasma

136-145

3.5-5.0

98-105

280-300

--

5% dextrose

0

0

0

278

--

Dextrose saline 0.18%

30

0

30

283

--

Normal saline 0.9%

154

0

154

308

0.2

Ringer’s lactate

130

4

109

273

0.2

Hartman’s

131

5

111

275

0.2

Gelatin 4%

145

0

145

290

1-2

5% albumin

150

0

150

300

2-4

HES 6% 130/0.4

154

0

154

308

4-8

 

Composition of commonly used intravenous solutions. HES (hydroxyethyl starch)

 

 

*9) E

*10) D

 

In patients without disorders of gastric emptying undergoing elective surgery clear non-particulate oral fluids should not be withheld for more than two hours prior to the induction of anaesthesia.

 

In the absence of disorders of gastric emptying or diabetes, preoperative administration of carbohydrate rich beverages 2-3 h before induction of anaesthesia may improve patient well being and facilitate recovery from surgery. It should be considered in the routine preoperative preparation for elective surgery.

 

Preoperative oral administration of solutions of carbohydrate oligomers has been shown in several trials to attenuate preoperative thirst, anxiety and postoperative nausea and vomiting. It also substantially reduces postoperative insulin resistance, thereby improving the efficacy of postoperative nutritional support.

 

*11) E

*12) D

  • Routine use of preoperative mechanical bowel preparation is not beneficial and may complicate intra and postoperative management of fluid and electrolyte balance. Its use should therefore be avoided whenever possible.

 

  • Where mechanical bowel preparation is used, fluid and electrolyte derangements commonly occur and should be corrected by simultaneous intravenous fluid therapy with Hartmann’s or Ringer-Lactate/acetate type solutions.

 

  • Excessive losses from gastric aspiration/vomiting should be treated preoperatively with an appropriate crystalloid solution which includes an appropriate potassium supplement. Hypochloraemia is an indication for the use of 0.9% saline, with sufficient additions of potassium and care not to produce sodium overload.

 

Losses from diarrhoea/ileostomy/small bowel fistula/ileus/obstruction should be replaced volume for volume with Hartmann’s or Ringer-Lactate/acetate type solutions. 

 

*13) C

 

Hypovolaemia due predominantly to blood loss should be treated with either a balanced crystalloid solution or a suitable colloid until packed red cells are available.

Hypovolaemia due to severe inflammation such as infection, peritonitis, pancreatitis or burns should be treated with either a suitable colloid or a balanced crystalloid.

The administration of large volumes of colloid without sufficient free water (e.g. 5% dextrose) may precipitate a hyperoncotic state.

 

*14) C

*15) D

Post-operative handling of sodium & water load

 

For the surgical patient it is even more difficult to excrete a salt and water load and to maintain normal serum osmolarity for several reasons.

 

  • The stress response to surgery causes anti-diuresis and oliguria mediated by ADH, catecholamines and the Renin-Angiotensin-Aldosterone System (RAAS).

 

Following surgery, even when the serum osmolarity is reduced by administration of hypotonic fluid, the ability to excrete free water is limited because the capacity of the kidney to dilute, as well as to concentrate urine, is impaired. Excess free water infusion risks dilutional hyponatraemia.

 

*17) A

If saline is infused, chloride overload accompanies sodium overload, and hyperchloraemia causes renal vasoconstriction and reduced GFR, further compromising the ability of the kidney to excrete sodium and water.

 

*18) C

*19) A

  • In more seriously ill surgical catabolic patients with increased urea production, there is a reduced ability to concentrate urine. As a consequence it requires two or more times the normal volume of urine to excrete a sodium and chloride load given in the perioperative period. Sodium and chloride excretion competes with excretion of nitrogen mobilised by the inflammatory response to surgery. A large proportion of the administered sodium, chloride and water is therefore retained as interstitial oedema.
  • Potassium depletion, due both to RAAS activity and the cellular loss of potassium which accompanies protein catabolism, reduces the ability to excrete a sodium load.
  • A sustained increase in systemic capillary permeability allows albumin and its attendant fluid (18 ml for every gram of albumin) to leak into the interstitial space, thereby worsening interstitial oedema. This exacerbates intravascular hypovolaemia and sodium and water retention by activation of the RAAS and secretion of ADH.
  • Intracellular sequestration of sodium and fluid due to lack of intracellular energy and failure of the cellular Na/K ATPase pump may occur in trauma, shock and fasting/malnutrition. In severe cases this gives rise to the so-called sick cell syndrome

 

*20) C

Nutritional status

 

  • Nutritionally depleted patients need cautious refeeding orally, enterally or parenterally, with feeds supplemented in potassium, phosphate and thiamine. Generally, and particularly if oedema is present, these feeds should be reduced in water and sodium. Though refeeding syndrome is a risk, improved nutrition will help to restore normal partitioning of sodium, potassium and water between intra- and extra-cellular spaces.

Surgical patients should be nutritionally screened, and NICE guidelines for perioperative nutritional support adhered to. Care should be taken to mitigate risks of the refeeding syndrome.

 

*21) A

 

Nutritionally depleted patients need cautious re-feeding orally, enterally or parenterally, with feeds supplemented in potassium, phosphate and thiamine. Generally, and particularly if oedema is present, these feeds should be reduced in water and sodium. Though re-feeding syndrome is a risk, improved nutrition will help to restore normal partitioning of sodium, potassium and water between intra- and extra-cellular spaces.

 

Surgical patients should be nutritionally screened, and NICE guidelines for perioperative nutritional support adhered to. Care should be taken to mitigate risks of the re-feeding syndrome.

 

Potassium is the dominant intracellular and sodium the dominant extracellular cation, but because in severe illness or malnutrition there is impairment of the Na/K ATPase pump, sodium tends to move into the cells and K out, a process which is related to surgical mortality. Conversely, re-feeding the depleted patient is associated with rapid cellular uptake of potassium and phosphate and exhaustion of limited thiamine stores leading to the re-feeding syndrome unless appropriate supplements of potassium, phosphate and thiamine are given. NICE criteria for identifying patients at risk of re-feeding syndrome.

 

*22) B

 

NICE criteria for nutritional support.

 

  • Nutritional support should be by the safest, simplest, most cost effective approach acceptable to the patient.
  • Favour oral over enteral and enteral over parenteral feeding.
  • Nutrition support should be considered in people who are malnourished, as defined by any of the following:
  • A BMI of less than 18.5kg/m2
  • Unintentional weight loss greater than 10% within the last 3-6 months
  • A BMI of less than 20kg/m and unintentional weight loss greater than 5% within the last 3-6 months.

 

  • Nutrition support should be considered in people at risk of malnutrition as defined by any of the following

 

  1. Have eaten little or nothing for more than 5 days and/or are likely to eat little or nothing for the next 5 days or longer
  2. Have a poor absorptive capacity, and/or have high nutrient losses and/or increased nutritional needs from causes such as catabolism.

 

*23) D

 

Defined as urine output < 0.5ml/kg/h

 

 

*24) B

 

Post-operative hyponatraemia

 

  • Up to 20% of women who develop symptomatic hyponatraemia die or suffer serious brain damage
  • Caused by surgical stress resulting in a syndrome of inappropriate antidiuretic hormone secretion and promoting water retention for several days
  • Women are more affected than men, as a result of their smaller fluid volume and other sex related hormonal factors
  • Premenopausal women are prone to brain damage at sodium concentrations below 128 mmol/l
  • Postmenopausal women do not usually become symptomatic until sodium concentrations have fallen below 120 mmol/l but may be symptomatic at higher levels if the rate of change is rapid
  • Ageing impairs fluid homoeostasis and increases the risk of severe hyponatraemia. This is compounded by chronic diseases and long-term use of drugs such as thiazide diuretics.
  • The risk of hyponatraemia is further increased by routine infusions of isotonic dextrose. Post-operative patients metabolise glucose almost immediately.
  • Isotonic dextrose infusions are effectively just water and volumes as low as 3-4 L over two days may cause convulsions, respiratory arrest, permanent brain damage, and death in healthy women

However, post-operative hyponatreamia also occurs even after infusion of near-isotonic solutions only (sodium chloride, 154 mmol/L, or Ringer lactate [sodium, 130 mmol/L, and potassium, 4 mmol/L])

 

*25) E

 

Typical features of post-operative hyponatreamia include

 

  • Hyponatraemia and low plasma osmolarity
  • Persistent excretion of hypertonic urine
  • Otherwise normal renal function (normal urea and creatinine)
  • Normal adrenal function
  • No evidence of extracellular fluid volume contraction (dehydration / hypotension)

Improvement of hyponatreamia following fluid restriction

 

*26) C

 

Post-op hyponatraemia

 

Early symptoms include:

  • Weakness
  • Nausea
  • Vomiting
  • Headache

 

Late symptoms include

  • Confusion and restlessness
  • Convulsions
  • Drowsiness
  • Eventually, coma and respiratory arrest

 

Typically, patients have an initial uncomplicated post-operative recovery followed by symptoms of hyponatraemic encephalopathy

 

*27) D

 

Typical features of post-operative hyponatreamia include

 

  • Hyponatraemia and low plasma osmolarity
  • Persistent excretion of hypertonic urine
  • Otherwise normal renal function (normal urea and creatinine)
  • Normal adrenal function
  • No evidence of extracellular fluid volume contraction (dehydration / hypotension)
  • Improvement of hyponatreamia following fluid restriction

 

Early symptoms include:

  • Weakness
  • Nausea
  • Vomiting
  • Headache

 

Late symptoms include

  • Confusion and restlessness
  • Convulsions
  • Drowsiness
  • Eventually, coma and respiratory arrest

 

Typically, patients have an initial uncomplicated post-operative recovery followed by symptoms of hyponatraemic encephalopathy

 

*28) A

 

Factors contributing to inappropriate ADH secretion in the post-operative period

 

  1. Pre-operative fasting: dehydration results in increased ADH secretion
  2. Pain & emotional stimuli: shown to increase ADH secretion. ADH levels shown to be increased by incision and stimulation of the pleura and peritoneum
  3. Haemorrhage: results in reduction of circulatory volume and stimulation of ADH secretion
  4. General anaesthesia: general anaesthetics produce an acute fall in GFR and urine volume with an increase in ADH secretion

Drugs: opiates and barbiturates increase ADH secretion

 

*29) C

 

Treatment options

 

  1. Fluid restriction to 1.5-2 L normal saline per 24h with sodium levels monitored every 2h. The aim is to raise serum sodium by 1-2 mmol/l per hour
  2. Hypertonic saline may be used but closer monitoring should be undertaken as a rapid rise in sodium concentration may lead to osmotic demyelination
  3. A loop diuretic such as furosemide may be used to enhance free water excretion and hasten the restoration of normal sodium concentrations