	Useful	Not so useful
Clinical examinations	BP (especially postural or post-exercise drop)	Skin turgor
	Oedema	Eye turgor
	JVP	Mucous membranes
	Peripheral perfusion
	Pulse
	Basal crackles
Charts	Serial weight (on same machine)	Fluid balance (input/output)
Additional tools	CVP line – use dynamically	CVP – absolute
	CXR	Urine Na⁺
	Pulmonary artery flow catheter	Osmolality

Case history (1)

A 43-year-old man is brought to A&E with a 4-day history of severe abdominal pain and watery diarrhoea up to 10 times daily. He has felt so bad that he has hardly drunk or eaten anything over the last few days. He has lost 5 kg in weight.

He is normally fit and well and he wonders whether he has some form of severe gastroenteritis.

On examination he is dehydrated with dry tongue. Abdominal examination reveals some generalised tenderness.

Figure 9.1 (a) shows the other signs of hypovolaemia.

Remember

• Examine the patient again!

• Then again later (today)!!

• And again (tomorrow)!!!

Laboratory tests are no substitute for clinical assessment.

Case history (2)

A 24-year-old man is involved in an RTA, receiving injuries to his chest and abdomen.

On admission to the Trauma Unit he is shocked, with a tachycardia of 120 bpm, BP 90/55 and cold, clammy peripheries. His GCS score is 12.

Examination of his chest reveals a right haemothorax. Abdominal examination shows a tender, rigid abdomen with no bowel sounds, suggestive of peritonitis.

Management

Airways, circulation and breathing were quickly assessed and ventilation started with a very tight-fitting facial mask.

Intravenous access was achieved with a large bore intravenous cannula and 0.9% saline started. A urinary catheter was inserted.

An emergency CT scan confirmed the haemothorax and an intercostal tube drain was inserted.

Abdominal CT confirmed free fluid in the abdomen and an abnormal small intestine, suggestive of ischaemia. Liver, spleen and other organs seemed normal.

A CVP line was inserted to assess fluid balance. Fluid challenge (Table 9.2 and Fig. 9.2) indicated hypovolaemia, and blood transfusion (2 units) was started with repeated checks on his fluid status.

Table 9.2 Fluid challenge

Use CVP dynamically (Fig. 9.2). Take reading

↓

Give IV bolus (100 mL 0.9% saline) fluid challenge

There is no absolute value

Do this yourself! If done correctly this gives accurate information

Figure 9.2 Fluid challenge.

A laparotomy was performed and 20 cm of small bowel resected.

On post-op, his vital signs were stable but he had not passed urine despite intravenous furosemide and adequate fluid replacement. His urea and creatinine have risen, indicating acute kidney injury due to acute tubular necrosis.

Further management is provided by the Renal Unit with the aim of controlling fluid and electrolyte balance, and treatment of sepsis until the kidneys spontaneously recover. After 10 days’ management, including haemofiltration (necessary for uncontrolled hyperkalaemia), he started to pass urine and eventually made a good recovery.

Fluid balance and electrolytes: sodium problems

What are you actually measuring when you measure the serum sodium?

A ratio of:

• Extracellular Na⁺ in mmol

• Extracellular water in litres.

Using this concept you can describe how serum Na⁺ becomes abnormally low (hyponatraemia) or high (hypernatraemia) (Table 9.3).

Table 9.3 Hyponatraemia and hypernatraemia

Ratio (Na⁺ : water)	Extracellular water
Hyponatraemia
Water ↑	→ or ↓
Water ↑ > Na⁺ ↑	↓↓
Na⁺ ↓	↓
Hypernatraemia
Water ↓	→ or ↓
Water ↓ > Na⁺ ↓	↓↓
Na⁺ ↑	↑

How do I work out why?

The key is to determine the extracellular water. Examine the patient (see Fig. 9.1).

Hyponatraemia

This is defined as sodium < 135 mmol/L.

Case history

The gynaecology SHO is worried about a 53-year-old woman who is 3 days post-op after a transabdominal hysterectomy. Her serum Na⁺ has fallen to 123 mmol/L. The SHO asks whether the woman should be given some 1.8% (twice-normal) saline? The polite answer is No!

Remember

Wherever sodium goes, water is sure to follow, and vice versa.

Management

• Fluid assessment

• Examine fluid charts.

On examination there were no features of fluid depletion, which excludes true Na⁺ depletion.

You then discover that she had been receiving 5% glucose by IV infusion since surgery 3 days ago. This is probably the most common cause of hyponatraemia in a surgical patient.

Action

• Stop IV fluids, restrict oral fluids to 1 litre daily and food as requested by the patient. 48 hours later her serum sodium is 132 mmol/L.

Other causes of hyponatraemia

• Diuretic therapy: particularly loop diuretics cause large renal losses of salt and water and metabolic alkalosis.

• Severe heart failure, advanced liver cirrhosis or nephrotic syndrome: hyponatraemia with increased total body sodium and even greater excess of water resulting in ascites and oedema. Plasma osmolality is low. Increased water orally continues in the face of salt restriction, diuretic therapy or both and will aggravate the ascites and oedema.

• Syndrome of inappropriate ADH production (p. 459).

• Pseudohyponatraemia: e.g. hyperlipidaemic states where sodium is confined to the aqueous phase or monoclonal gammopathies, hyperglycaemia (10 mmol rise reduces sodium by approximately 2 mmol).

Hypernatraemia

Case history

A 47-year-old man is in the Neurosurgical Unit, having had a pituitary tumour removed by trans-splenoidal surgery. He has made a normal postoperative recovery but on review prior to discharge he complains of excess thirst and nocturia.

Review of the fluid balance charts show that he is drinking nearly 5 litres a day, with a urinary output of 3.5 L.

Recent blood tests show a serum Na⁺ of 153 mmol/L.

You diagnose cranial diabetes insipidus which you know occurs transiently for a few days or weeks after pituitary surgery.

Hypernatraemia is defined as sodium > 145 mmol/L.

• Iatrogenic: IV infusion of hypertonic sodium bicarbonate, hyperalimentation by IV route or nasogastric tube, sodium chloride tablets, sea water drowning or mineralocorticoid excess; total body sodium is elevated in these conditions. Signs are of hypervolaemia.

• Impaired thirst/unconscious patient: total body sodium is low because of both sodium and water deficit but water losses are greater than the losses of sodium. Signs are of hypovolaemia.

• Osmotic diuresis, e.g. diabetic ketoacidosis, radiocontrast, mannitol: total body sodium is low because of both sodium and water deficit, but water losses are greater than sodium losses. Urine is not maximally concentrated despite hyperosmolar state, in contrast to GI losses of sodium and water where urine is maximally concentrated. Signs here are of hypovolaemia.

• Water loss, e.g. diabetes insipidus: normal total body sodium. Signs are of euvolaemia.

Remember

True Na⁺ overload is invariably iatrogenic and gives a clinical picture of fluid overload.

Treatment

• Reassure the patient

• Avoid rapid correction (Fig. 9.3). Serum Na⁺ should not fall > 1 mmol every 2 hours, i.e. 10 mmol/24 hours.

• Initially give IV 0.45% saline. This is followed by 5% glucose with 20 mmol/L K⁺ with frequent monitoring of volume status and serum Na⁺ level. This stays in the extracellular compartment (see assessing fluid status, p. 223).

Figure 9.3 Effect on the brain of changes in sodium concentration.

Key points

• Examine the patient: know where their water is.

• Slow correction.

• Hyponatraemia is a more common problem in clinical practice than hypernatraemia.

• Hypernatraemia is generally found in ITU patients.

Patient stopped passing urine

Information

• Oliguria: urine output < 500 mL/day

• Anuria: urine output < 50 mL/day

Case history

The surgical house officer calls you at 10 p.m. to say that she has a 62-year-old man who is 2 days post-laparotomy and who isn’t passing urine.

What should you do?

• Do: see the patient.

• Don’t: simply give telephone advice.

Take a detailed history of type of surgical procedure. Ask about GI bleeding, dehydration or other fluid losses, nephrotoxic drugs, drugs associated with hypersensitivity reaction causing tubo-interstitial nephritis (e.g. penicillins, NSAIDs, cephalosporins), evidence of previous renal insufficiency, and any radiological procedure with contrast enhancement. Anuria usually means obstructive uropathy or vasculitides rather than acute tubulo-nephritis (ATN); evidence of these conditions should be sought.

On examination the patient has a tachycardia of 110 bpm with a low BP 90/50.

Examination of his abdomen shows a healing laparotomy scar, no tenderness and no evidence of a palpable bladder.

Common causes of poor urinary output

• Urine retention: always catheterise.

• Dehydration: assess fluid status (see Fig. 9.1). Look at fluid balance charts.

• Shock: see Table 9.4.

• Drugs: look at medicines chart.

Table 9.4 Shock – failure of organ perfusion

Results in this man

• No urine from catheter

• Your clinical assessment – hypovolaemic

• Fluid charts incorrectly filled in but patient seems to have received 2 litres of fluid (intravenous and oral) over the last 48 hours.

Initial management

This man is fluid depleted and needs fluid replacement (Table 9.5):

• 0.9% saline IV ( 20 mmol/K⁺) added to each litre

• Write up initial regimen: modulate according to patient age, size and severity

• Reassess fluid status regularly

• When in doubt use a CVP line.

Table 9.5 Fluid replacement

Modified from Kumar and Clark Clinical Medicine 8th edn, 2012.

Aim

To establish a diuresis of at least 100 mL per hour. In most cases, a failure to achieve this is because of inadequate fluid replacement.

Other actions

• U&Es

• Stop potentially nephrotoxic drugs

• Stop anti-hypertensive drugs

• Ask nurses to record daily weights and to make careful note of fluid intake and urine output on the fluid chart.

Still no urine?

• Are you certain the patient is adequately fluid replete?

• Check that the urine catheter is not blocked or misplaced.

• Give a loop diuretic, e.g. furosemide.

• The patient might now have established acute kidney injury. Refer to nephrologist.

Fortunately this man responded to fluid replacement and produced urine, intitially 50 mL/hour.

Key points

• Don’t miss urine retention.

• Recognise shock.

• Assess fluid status regularly.

• Most cases will need fluid replacement, and failure to achieve this can result in established renal failure.

Acute heart failure

Acute heart failure occurs when cardiac function falls, causing elevated cardiac filling pressure. This causes severe breathlessness with fluid accumulating in the interstitial and alveolar spaces of the lung (pulmonary oedema).

Case history

A 65-year-old, 50-kg woman who smokes 20 cigarettes per day and with a past history of intermittent claudication, presented to A&E with acute shortness of breath. She is on no medication.

On examination she was centrally and peripherally cyanosed, and peripherally cold and clammy, with a raised JVP, gallop rhythm and bilateral coarse crackles up to both mid-zones. She had absent foot pulses and bilateral femoral bruits. Her BP at presentation was 195/98.

Her ECG showed hypertensive changes (with left ventricular hypertrophy) and a CXR showed bilateral perihilar shadowing. Initially, her biochemistry was:

• Na: 142 mmol/L

• K: 3.1 mmol/L

• Urea: 12 mmol/L

• Creatinine: 115 µmol/L. eGFR 44 mL/min/1.73 m².

What has gone wrong?

It is very likely that she has developed acute kidney injury. This is because she has underlying renovascular disease.

RIFLE criteria for acute kidney injury

Grade	GFR Criteria	UO Criteria
Risk	SCr × 1.5 or GFR decrease >25% (within 48 hr)	UO < 0.5 mL/kg/h × 6 h
Injury	SCr × 2 or GFR decrease >50%	UO < 0.5 mL/kg/h × 12 h
Failure	SCr × 3, GFR decrease >75%,	UO < 0.3 mL/kg/h × 24 h
	SCr > 350 µmol/L
	with an acute rise > 40 µmol/L
Loss	Persistent AKI > 4 weeks
ESKD	Persistent ESKD > 3 months

SCr = serum creatinine; UO = Urinary output; ESKD = end stage kidney disease.

(Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Lancet 2012; 380: 756–766.

There is a new consensus definition that merges RIFLE criteria and the Acute Kidney Injury network definition (Kidney Disease Improving Global Outcomes (K-DIGO) group 2012).