Critical Care Kanani

Question 1

Which abdominal organs are most commonly injured?

Answer 1

The three most commonly injured organs are the liver, spleen and kidneys.

Question 2

Investigating abdominal trauma

Answer 2

The initial investigations performed to assess the abdomen as a whole are:
-Plain radiography: also assesses the bony pelvis
-Ultrasound: particularly good for the presence of free
fluid in the abdomen, or haematoma around solid organs. There is a 10% risk of missing a significant injury
-Diagnostic peritoneal lavage (DPL): this is 98% sensitive for intra-peritoneal bleeding
-CT scanning: this can be used if the results of the DPL are equivocal, and may also be performed at the same time as a brain scan. Very good for retroperitoneal injury, less so for hollow viscus injury such as the bowel

Question 3

Under which circumstances would you perform a diagnostic peritoneal lavage (DPL)?

Answer 3

Some of the indications are:
- A suspicion of abdominal trauma on clinical examination
- Unexplained hypotension: with the abdomen being the
source of occult haemorrhage
- Equivocal abdominal examination because of head injury
and reduced level of consciousness
- The presence of a wound that has traversed the
abdominal wall, but there is no indication for immediate laparotomy, e.g. a stab wound in a stable patient

Question 4

When is DPL contraindicated?

Answer 4

The most important contraindication for DPL is in the situation which calls for mandatory laparotomy, e.g. frank peritonitis following trauma, abdominal gunshot injury or a hypotensive patient with abdominal distension.

Question 5

What are the positive criteria with DPL?

Answer 5

• Lavage f luid appears in the chest drain or urinary catheter
• Frank blood on entering the abdomen
• Presence of bile or faeces
• Red cell count of

Question 6

Acid base balance organs

Answer 6

The main organ systems involved in regulating acid-base balance are:

• Respiratory system: this controls the pCO2 through alterations in alveolar ventilation. Carbon dioxide indirectly stimulates central chemoceptors (found in the ventro-lateral surface of the medulla oblongata) through through H+ released when it crosses the blood-brain barrier (BBB) and dissolves in the cerebrospinal f luid (CSF)
• Kidney: this controls the [HCO3-], and is important for long term control and compensation of acid-base disturbances
• Blood: through buffering by plasma proteins and haemoglobin
• Bone: H+ may exchange with cations from bone mineral. There is also carbonate in bone that can be used to support plasma HCO3 levels
• Liver: this may generate HCO3 and NH4 (ammonia)
  by glutamine metabolism. In the kidney tubules, ammonia excretion generates more bicarbonate

Question 7

How does the kidney absorb bicarbonate?

Answer 7

There are three main methods by which the kidneys increase the plasma bicarbonate:

• Replacement of filtered bicarbonate with bicarbonate
  that is generated in the tubular cells
• Replacement of filtered phosphate with bicarbonate that
  is generated in the tubular cells
• By generation of ‘new’ bicarbonate from glutamine that is
  absorbed by the tubular cell

Question 8

Define the base deficit.

Answer 8

The base deficit is the amount of acid or alkali required to restore 1l of blood to a normal pH at a pCO2 of 5.3kPa and at 37°C. It is an indicator of the metabolic component to an acid-base disturbance. The normal range is -2 to +2

Question 9

What are the major ‘renal’ causes of acute renal failure?

Answer 9

• Acute tubular necrosis
• Glomerulonephritis
• Interstitial nephritis
• Bilateral cortical necrosis
• Reno-vascular: vasculitis, renal artery thrombosis
• Hepatorenal syndrome

Question 10

What is acute tubular necrosis?

Answer 10

Acute tubular necrosis is renal failure resulting from injury to the tubular epithelial cells, and is the most important cause of acute renal failure. There are two types:

• Ischaemic injury: following any cause of shock with resulting fall in the renal perfusion pressure and oxygenation
• Nephrotoxic injury: from drugs (aminoglycosides, paracetamol), toxins (heavy metals, organic solvents), or myoglobin (from rhabdomyolysis)

Question 11

What are the major ‘post-renal’ causes?

Answer 11

Acute obstruction from calculi
- Obstruction from tumours arising from the renal
parenchyma or transitional epithelium of the
pelvi-calyceal system
- Extrinsic compression from pelvic tumours
- Iatrogenic injury, e.g. inadvertent damage to the ureters
during bowel surgery
- Prostatic obstruction
- Increased intra-abdominal pressure (>30 cmH2O)

Question 12

Which part of the kidney is the most poorly perfused?

Answer 12

The renal medulla is more poorly perfused than the cortex. This ensures that the medullary interstitial concentration gradient formed by tubular counter current multiplication is preserved and maintained.

Question 13

Which part of the nephron is the most susceptible to ischaemic injury, and why?

Answer 13

The cells of the thick ascending limb are the most susceptible to ischaemic injury for two important reasons

• The cells reside in the medulla, which has poorer oxygenation than the cortex
• The active NaKTPase pumps at the cell membrane have a high oxygen demand.

Question 14

Name some common drugs of surgical importance that may exacerbate or cause acute renal failure.

Answer 14

• Paracetamol: overdose is a known cause of acute tubular
  necrosis
• Non-steroidal anti-inflammatory drugs: can lead to renal failure by reducing the renal protective effects of prostaglandins during renal ischaemia
• Aminoglycosides: a potent cause of acute tubular necrosis
• Penicillins: can cause interstitial nephritis
• Furosemide: can lead to interstitial nephritis
• Dextran 40: a colloid used during f luid resuscitation

Question 15

What are the two most important life-threatening complications of renal failure?

Answer 15

• Acute pulmonary oedema: due to fluid retention with
  over-hydration
• Hyperkalaemia: leading to metabolic acidosis and cardiac arrhythmias
  Both may require urgent dialysis as part of the management.

Question 16

ARDS definition

Answer 16

ARDS is a syndrome of acute respiratory failure with the formation of a non-cardiogenic pulmonary oedema leading to reduced lung compliance and hypoxaemia which is refractory to oxygen therapy. The changes are seen as:
Diffuse pulmonary infiltrates seen on chest radiography
- Pulmonary wedge pressure of of

Question 17

How does it relate to ‘acute lung injury’ and the ‘systemic inflammatory response syndrome’?

Answer 17

Acute lung injury (ALI) comprises of a number of non-specific pathological changes in the lung in response to a specific insult.

These changes are like that of ARDS, but of decreased severity in that the PaO2/FiO2 is

Question 18

Causes of ARDS

Answer 18

The triggering factors can be organised into a number of groups:
- Pulmonary insults:
- Trauma
- Pneumonia
- Aspiration
- Smoke inhalation
- Fat embolism
- Multiple trauma
- Generalised sepsis
- Others: massive transfusion, disseminated intravascular
coagulation (DIC), acute pancreatitis, cardio-pulmonary bypass

Question 19

What is the mechanism of action of nitric oxide?

Answer 19

Nitric oxide, (‘endothelium-derived relaxing factor’) is an activator of the cytoplasmic enzyme guanylyl cyclase. This increases the intracellular cyclic guanosine monophosphate (cGMP) levels, which stimulates a cGMP-dependent protein kinase. This activated protein kinase stimulate the phosphoryla- tion of key proteins in a pathway that leads to a relaxation of vascular smooth muscle cells.

Question 20

Ramsay scoring system for sedation

Answer 20

There are a number of techniques in routine clinical use to determine the level of sedation attained. The most com- monly employed of these is the Ramsay scoring system that describes six levels of sedation

Question 21

Sedation drugs

Answer 21

The most commonly used classes of drugs are
- Benzodiazepines: e.g. diazepam and midazolam
- Intravenous (i.v.) anaesthetic agents: such as propofol and ketamine
- Inhalational anaesthetic: nitrous oxide (70%)
- Opiate analgesics: morphine and the synthetic opioids pethidine and fentanyl are popular choices. They may be combined effectively with benzodiazepines
- Trichloroethanol derivatives: such as chloral hydrate
- Butyrophenones: e.g. haloperidol. As a group they are
neurotransmitter-blocking drugs
- Phenothiazines: e.g. chlorpromazine. They also act on neurotransmitter receptors

Question 22

The most commonly used sedative drug

Answer 22

The most commonly used sedative drugs are propofol, benzodiazepines and the opioid analgesics.

Question 23

major physiological side effect of propofol?

Answer 23

major physiological side effect of propofol?
The important side effect of propofol is hypotension on induction, and is caused by a fall in the systemic vascular resist- ance and/or myocardial depression. As with many of the other sedatives, it also leads to respiratory depression.

Question 24

Give some examples of the opiates in common use. Which are the synthetic and non-synthetic agents?

Answer 24

The commonly used opiates are
- Non-synthetic: morphine, codeine (10% of this is
metabolised to morphine)
- Semi-synthetic: diamorphine, dihydrocodeine
- Synthetic: pethidine, fentanyl

Question 25

Which receptor do opiate analgesics act on?

Answer 25

The majority of the effects of the opiates are carried out through the mu-receptor. They may also have some action through the other two types of opiate receptors, kappa and delta.

Question 26

What are the systemic effects of the opiates?

Answer 26

The effects of the opiates are
- Analgesia: they are good for moderate to severe pain of
any cause and modality. Less effective for neuropathic pain, such as phantom limb pain, or allodynia (pain from a non-painful stimulus)
- Respiratory depression: with blunting of the ventilatory response to rising pCO2. Also causes suppression of the cough ref lex, both of which encourage sputum retention, atelectasis and pneumonia in the critically ill
- Sedation: with a reduction in the level of consciousness with higher doses, so beware in those with head injuries
- Nausea and vomiting: following stimulation of the chemoreceptor trigger zone in the area postrema
- Reduced GI motility: which leads to constipation
- Euphoria
- Dependence and tolerance: there is a progressively reduced effect from the same dose of drug
- Histamine release from mast cells: producing pruritis and reduced systemic vascular resistance

Question 27

Why is morphine not advocated for use in

abdominal pain of biliary origin?

Answer 27

Why is morphine not advocated for use in
abdominal pain of biliary origin?
Morphine increases the tone of the sphincter of Oddi (as well other sphincteric muscles), while stimulating contraction of the gallbladder. Therefore, it can exacerbate biliary pain.

Question 28

What are the therapeutic effects of paracetamol (acetaminophen)?

Answer 28

What are the therapeutic effects of paracetamol (acetaminophen)?
This is an analgesic and anti-pyretic with minimal anti- inf lammatory properties.

Question 29

By what mechanism does overdose cause liver injury?

Answer 29

By what mechanism does overdose cause liver injury?
The cause of liver injury lies with the metabolism of para- cetamol. Normally it is conjugated in the liver, with the production of a small amount of the toxic metabolite N-acetyl- benzoquinoneimine. Binding to hepatic glutathione renders this metabolite harmless.With overdose, glutathione is depleted, leading to hepatocyte injury. Acetylcycteine, the drug used to treat overdose, is a glutathione precursor.

Question 30

How do the non-steroidal anti-inflammatory

drugs (NSAIDs) work?

Answer 30

How do the non-steroidal anti-inflammatory
drugs (NSAIDs) work?
These agents act to reduce prostaglandin formation by the inhibition of the enzyme cyclo-oxygenase which acts on arachidonic acid. This leads to a modif ication of the inf lam- matory reaction and its effects on the stimulating nociception.

Question 31

NSAID side effects

Answer 31

What are NSAIDs systemic side effects?
The systemic side-effects of these agents include
- Gastrointestinal: dyspepsia, gastritis and peptic ulceration.
There is direct stimulation of acid secretion by the gastric parietal cells, with reduced bicarbonate and mucus production
- Renal: may precipitate acute renal failure, especially in those with pre-existing renal suppression, dehydration or hypotension. Also leads to salt and water retention
- Coagulopathy: inhibition of platelet thromboxane A2 production leads to their reduced ability to aggregate and form the primary platelet plug. This is a permanent effect, and is reversed only when new platelets are formed
- Bronchospasm: the inhibition of cyclo-oxygenase leads to arachidonic acid being metabolised down the pathway of leukotriene formation, which induce brochospasm

Question 32

How is renal injury precipitated?

Answer 32

How is renal injury precipitated?
There is inhibition of compensatory PGI2 and PGE2 formation that occurs during situations of reduced renal perfusion. These prostaglandins normally promote vasodilatation during such situations, offsetting the development of acute tubular necrosis.

Question 33

Some of the systemic effects of epidurals include

Answer 33

Some of the systemic effects of epidurals include:
- Hypotension: due to block of the sympathetic outflow
causing peripheral vasodilatation
- Reduced cardiac output may occur due to a reduction in
the venous return
- Attenuation of the surgical stress response
- Reduction of the functional residual capacity
- Reduction of post-operative deep venous thrombosis: due
to a number of causes including the concomitant use of i.v. fluids used to support the arterial pressure

Question 34

Stanford or DeBakey systems aortic dissection

Answer 34

Aortic dissections may be classified according to the Stanford or DeBakey systems:

Stanford
-Type A: dissection involves the ascending aorta only
-Type B: involves the descending aorta with or without
the ascending aorta
DeBakey
-Type I: involves the ascending aorta, arch and descending aorta
-Type II: confined to the ascending aorta
-Type III: conf ined to the descending aorta, beyond the
origin of the subclavian artery

Question 35

What are the pathological hallmarks of dissection?

Answer 35

The recognised findings on microscopy are

• Myxoid degeneration: loss of elastic fibres and replacement of the musculo-elastic tissue with a proteoglycan-rich matrix
• Cystic medial necrosis: may be associated with injury or occlusion of the vasa vasorum

Question 36

In which plane of cleavage does the dissection propagate down the aorta?

Answer 36

Although initially commencing as an intimal tear, the dissec- tion propagates along the plane that runs between the inner 2/3 and outer 1/3 of the media.

Question 37

Which conditions predispose to aortic dissection?

Answer 37

The predisposing factors are
- Inherited defects:
- Marfan’s syndrome: there is defective cross-linking of collagen
- Ehlers-Danlos syndrome: defective procollagen formation
- Pseudoxanthoma elasticum: fragmentation of elastic fibres in the media
- Hypertension: leading to increased shearing forces across the intima
- Pregnancy: associated with microscopic changes in the media
- Bicuspid aortic valve
- Traumatic injury to the aorta
- Iatrogenic: cardiac catheterisation, aortic cannulation at
cardiac surgery, aortic valve replacement

Question 38

Effects of aortic dissection

Answer 38

Dissection can lead to a number of outcomes Dissection can lead to a number of outcomes
- Propagation to the abdominal aorta, leading to gut
ischaemia if the mesenteric vessels are involved, or renal
failure if the renal vessels are involved
- If the intercostal and lumbar vessels are occluded, then it
can lead to spinal cord ischaemia, due to loss of the supply
from the arteria radicularis magna
- Propagation along the carotid arteries, leading to stroke
- Involvement of the coronary ostia and coronary arteries:
leading to angina and myocardial infarction
- Involvement of the aortic valve ring, with the development
of acute aortic regurgitation
- Rupture into the pericardium, producing cardiac
tamponade
- Rupture into the pleura, producing a haemothorax
- Compression of surrounding structures: such as the trachea,
oesophagus or superior vena cava
- The dissection may re-enter the lumen through another
intimal tear, producing a double-barreled aorta

Question 39

Physical examination signs of aortic dissection

Answer 39

Some findings on physical examination
- The patient may exhibit signs of cardiogenic or
hypovolaemic shock
New diastolic murmur of aortic regurgitation
- Signs of cardiac tamponade: muff led heart sounds,
increased venous pressure, reduced arterial pressure and
pulsus paradoxus
- Asymmetric pulses and blood pressures
- Neurological signs: stroke or spinal cord involvement

Question 40

Aortic dissection treatment

Answer 40

The principles of management include
- Adequate resuscitation with f luids to maintain the
cardiac index and renal function. Following bladder catheterisation, a urine output of 30–40 ml/h must be maintained
- The fluids are given through wide-bore i.v. cannulae, from which samples can be taken for baseline investigations and a 10-unit cross match of blood
- A central-line should be inserted to help monitor the filling pressures
- The velocity of the ejection fraction and arterial pressure should be controlled with an infusion of labetalol. Sodium nitroprusside has also been used, but this can cause a ref lex tachycardia and increases the ejection velocity. This increases the shearing forces on the intima, propagating the dissection
- The patient should be transferred to a cardiothoracic unit when stable
- Surgery involves replacement of the diseased segment of the aorta with a prosthetic graft and re-implantation of the coronary arteries if the aortic root is involved
- Aortic root involvement also requires valve replacement or re-suspension
- If the arch is involved, deep hypothermic circulatory arrest is required during repair to preserve cerebral function
- For type B dissections, conservative management is advocated – surgery confers no added benefit
- In some instances, the dissection may be stented

Question 41

Why does a high-inspired concentration of oxygen lead to atelectasis?

Answer 41

The reason lies in the higher solubility and faster absorption of oxygen as compared with nitrogen.When inspiring air, the slowly absorbed nitrogen ‘splints’ the airways open as oxygen
is being absorbed. At a high FiO2, this nitrogen ‘splint’ is reduced or absent, so that when the oxygen is absorbed, the lung unit collapses. This is also called ‘absorption’ atelectasis.