Fluid Management

Question 1

u are called to surgical HDU to review a 60-year-old man who underwent anterior abdominoperoneal resection for the rectum under GA 12-hours-ago. The nursing staff are concerned about the UOP. Physical examination is unremarkable. The examiner will give you a fluid balance chart and obs chart

How would you manage this case?

What is the rationale for giving fluid challenge rather than speeding up the drip

Formula for fluid challenge

The patient is on 2 hours monitoring, is that adequate?

Answer 1

In view of response to previous fluid challenges, I will do more fluid challenges (250ml bolus or 10-20ml/kg)
as fast as possible and monitor the response

A fluid challenge is both therapeutic and diagnostic. It helps assess the patient’s responsiveness to fluids and prevents unnecessary fluid overload if the oliguria is not due to hypovolemia.

This is based on the Frank–Starling law, which states that increasing intravascular volume increases ventricular stretch and stroke volume — but only up to an optimal point. Beyond that, further fluid loading leads to congestion and pulmonary edema

Giving fluid slowly or just increasing drip rate:
• Doesn’t adequately stretch the ventricle → no real test of fluid responsiveness.
• Gives no diagnostic information about cardiac performance.
• May delay resuscitation in shock.

250 ml bonus or give 5ml/kg in cardiac pt, 10ml/kg in normotensive, 20ml/kg in hypotensive pt and monitor response

No, he should be monitored hourly

Question 2

is there any reason why synthetic colloids may not be desirable in postoperative pt?

How to manage this patient after fluid challenge / for the remainder of your shift?

Assuming the patient becomes more hemodynamically unstable and you have given him more fluid. How to assess the cardiovascular function and patient’s response to therapy?

Who to notify, when?

How blood pressure is calculated?

How to increase blood pressure?

Answer 2

1/ No evidence of benefit over crystalloids.
2/ More expensive.
3/ Risk of anaphylaxis.
4/ some (as starch) may lead to increase mortality in sepsis cases.
5. Risk of AKI
6.impair function of platelets and clotting factors

Post–fluid challenge, I’d reassess for improvement in perfusion, maintain close monitoring of vitals, urine output, and labs, and escalate promptly if there’s no response or worsening instability.
• Repeat fluid challenge if necessary
• Maintain high index of suspicion for other problems such as occult hemorrhage
• Leave instructions for nursing staff you contact me if they’re concerned

If the patient becomes more hemodynamically unstable after receiving fluids, I would assess cardiovascular function and the response to therapy using both static and dynamic parameters.

Static parameters include blood pressure, heart rate, urine output, capillary refill time, and central venous pressure — which help assess overall volume status.

Dynamic parameters include cardiac output, stroke volume, and systemic vascular resistance — which can be measured using advanced monitoring devices such as LiDCO, PiCCO, or a Swan–Ganz catheter to determine true fluid responsiveness.”

I will notify my consultant when no response to multiple fluid challenges

Blood pressure (BP) is the product of the cardiac output (CO) and the systemic vascular resistance (SVR). The CO is the product of the heart rate (HR) and stroke volume (SV)

Inotropic support and fluids to increase CO, vasopressor agents to increase SVR

Question 3

Hormonal changes in surgery or trauma

Where is ADH (vasopressin) produced and what factors stimulate its secretion?

Where in the kidney does ADH act?

Action of ADH

Answer 3

In response to surgical stress, there’s activation of the hypothalamic–pituitary–adrenal axis and sympathetic nervous system to preserve circulation and maintain perfusion.

↑ Increased hormones:
• Cortisol
• ACTH
• Aldosterone
• ADH (vasopressin)
• Renin
• Glucagon
• Growth hormone
• Prolactin

↓ Decreased hormones:
• Insulin (though insulin resistance increases)
• Testosterone
• Estrogen
• LH
• FSH

→ No significant change:
• TSH (may remain normal or slightly decreased)

Produced in the hypothalamus then transported, stored and released from the posterior pituitary Factors stimulating its secretion
• Reduce circulating volume
• Increased plasma osmolarity
• Angiotensin II

Collecting duct

Vasopressin»_space; Constrict arterioles»_space; increase peripheral vascular resistance
Increases the reabsorption of solute-free water by the collecting duct.

Question 4

By what mechanism does ADH facilitate reuptake of water from the tubular fluid?

Why does the water cross from the tubular fluid into the medulla?

What is the process by which the medullary tissue becomes hypertonic? / What are the mechanisms by which the kidneys increase osmolarity in the renal medulla?

How does aldosterone act to maintain circulating volume?

Answer 4

It stimulates water reabsorption by insertion of aquaporins (proteins) or “water channels” into the membranes of collecting ducts. These channels transport solute-free water through tubular cells and back into blood.

The renal medulla becomes hypertonic by the countercurrent multiplier mechanism of the Loop of Henle.

In this mechanism:
• The descending limb is permeable to water but not to solutes, so water moves out, concentrating the tubular fluid.
• The ascending limb is impermeable to water but actively pumps out sodium and chloride, which increases the osmolarity of the medullary interstitium.
• Because the limbs flow in opposite directions, this creates and multiplies a corticomedullary osmotic gradient.
• Urea recycling from the collecting duct further adds to medullary hypertonicity.
• The vasa recta act as a countercurrent exchanger to maintain this gradient without washing it out.”

Stimulates the reuptake of Na + by acting on the receptor at the junction between DCT and collecting duct.

Question 5

Actions of renin angiotensin aldosterone system (RAAS):

Answer 5

Actions of Angiotensin II

1.Angiotensin II causes arteriolar vasoconstriction, leading to an increase in both systolic and diastolic blood pressure.
2.It stimulates the adrenal cortex to secrete aldosterone, which enhances sodium and water reabsorption.
3.It also acts directly on the renal tubules to promote sodium reabsorption.
4.In the sympathetic system, it facilitates the release of noradrenaline, further contributing to vasoconstriction.
5.Within the kidney, it causes contraction of mesangial cells, thereby reducing the glomerular filtration rate (GFR).
6.In the brain, angiotensin II decreases baroreceptor sensitivity and stimulates thirst, antidiuretic hormone (ADH), and adrenocorticotrophic hormone (ACTH) release, all of which help conserve water and maintain elevated blood pressure.