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The Patient Involved in a Road Trac Collision
79
For which complications do you need to monitor
Danielle over the next 24–48 hours?
Pain–if she improves neurologically, pain can often be a signicant
factor in delaying recovery, especially with rib fractures where conserva-
tive management is usual. Careful titration of adequate opioid analgesia
can be very dicult in these types of patients. Consideration could be
given to using regional techniques.
Pneumonia and respiratory failure–pulmonary contusions, rib fractures
and mechanical ventilation itself can predispose patients to respiratory
tract infections. This may also lead to developing an acute respiratory
distress syndrome (ARDS).
Deep vein thrombosis–prophylactic techniques are usually divided into
mechanical and pharmacological methods. Antiembolism stockings and
pneumatic devices are associated with fewer complications but may not be
as eective as drugs. Although pharmacological methods (i.e. low molecular
weight heparins) are generally considered most eective, but their use must
be weighed against the risk of bleeding in the presence of traumatic injuries.
During the secondary survey, the nurse looking after Danielle asks you about
the relevance of the sternal fracture reported on the CT.
What would be your concerns regarding this nding?
Pain–sternal fractures are painful and will require adequate analgesia
when Danielle is awake, and when attempting to extubate. Pain control
will also need to be adequate to allow deep breathing and maintain her
ability to cough, to reduce the risk of a chest infection developing.
Blunt cardiac injury (BCI)–this should be considered in the presence of
a sternal fracture. Given the rapid deceleration mechanism associated
with road trac collisions, the myocardium can be exposed to signicant
shearing forces and compression between the sternum and vertebrae.
BCI should be considered in the presence of other signicant injuries
as it may remain a clinically silent entity (the diagnosis of BCI can be
particularly challenging).
How common is BCI?
A recent inspection of 15 976 patients (between 2007 and 2015) from the US
National Trauma Data Bank found that BCI was reported in less than 1% of patients.
Which types of trauma- related injuries are
associated with BCI?
Blunt force trauma resulting in sternal fracture or thoracic aortic injury is
strongly associated with BCI. Haemopneumothorax has been demonstrated
to be the strongest predictor for BCI in patients presenting with blunt force
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Clinical Cases in Critical Care
80
trauma. Any patient presenting with haemopneumothorax, sternal frac-
ture, injury to the oesophagus and/or thoracic aortic injury should ideally be
screened for BCI.
What are the myocardial patterns of injury
associated with BCI?
The most commonly reported injury associated with BCI is contusion. Usually, as
the right side of the heart lies anteriorly, it is most prone to BCI, with the reported
incidences of right atrial and right ventricle injury being 17–32% and 8–65% respec-
tively. Left-
sided chamber injuries are not as commonly reported. Patients who
rupture any of the four chambers of the heart are unlikely to survive to hospital.
Rarely, myocardial infarction may occur following injury to the coronary arteries.
How would you diagnose and evaluate BCI in
this patient?
Clinical suspicion needs to remain high in the presence of a massive haemo-
thorax and mechanism of blunt force trauma. Sternal fracture pain may be
confounded by other thoracic injuries (e.g. rib fractures) and reduced con-
sciousness. No gold standard exists to diagnose BCI. The following investiga-
tions are suggested:
Electrocardiography–a valuable screening tool, as the presence of ven-
tricular or atrial arrhythmias, conduction abnormalities (e.g. bundle
branch block) and ST segment abnormalities may suggest BCI. How-
ever, the absence or presence of abnormalities does not conclusively
rule out or rule in BCI.
Cardiac enzymes–being both highly specic and sensitive for myocar-
dial cell damage, troponin T may be elevated in the presence of BCI.
Following 6–8
hours from the time of injury, if the troponin levels remain
within normal limits, then BCI is highly unlikely.
Echocardiography–detection of abnormalities such as regional wall
motion abnormalities (RMWAs) or valvular dysfunction (e.g. regurgitant
jets) in patients who are unstable or have positive ECG ndings and/or
troponin levels may suggest BCI. Transoesophageal echocardiography
is usually more sensitive than the transthoracic approach, particularly
since chest wall injuries may degrade the quality of images using the
latter approach. Remember that in elderly trauma patients, the presence
of regurgitation or RWMAs may be pre- existing, especially in the context
of known ischaemic coronary disease.
Echocardiography does not demonstrate any anatomical abnormalities and
the ECG reveals sinus rhythm at a rate of 90 bpm. The troponin T level is
within normal limits. You and your team do not feel that Danielle has BCI.
Danielle improves following neurosurgical intervention, making a full
neurological recovery, and is successfully extubated on day 10 of admission.
She is stepped down to the neurosurgical ward and discharged home
2weeks later.
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The Patient Involved in a Road Trac Collision
81
Further reading
Advanced Trauma and Life Support®. Student Course Manual. (2018). Denitive
manual for dealing with patients presenting with trauma.
Roberts, I., Shakur, H., Coats, T. etal. (2013). The CRASH- 2 trial: a randomised
controlled trial and economic evaluation of the eects of tranexamic acid on death,
vascular occlusive events and transfusion requirement in bleeding trauma patients.
Health Technol. Assess. 17 (10). Original studies demonstrating the benet of using
tranexamic acid in trauma patients.
CRASH- 3 Trial Collaborators (2019). Eects of tranexamic acid on death, disability,
vascular occlusive events and other morbidities in patients with acute traumatic
brain injury (CRASH- 3): a randomised, placebo- controlled trial. Lancet. 394:
1713–1723.
Lichtenstein, D., Mezière, G., Lascols, N. etal. (2005). Ultrasound diagnosis of
occult pneumothorax. Crit. Care. Med. 33 (6): 1231–1238. Seminal paper on the use
of ultrasound to aid in diagnosing pneumothorax.
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6
Clinical Cases in Critical Care, First Edition. Alice Myers and Theophilus Samuels.
© 2023 John Wiley & Sons Ltd. Published 2023 by John Wiley & Sons Ltd.
Y
ou are asked to review an 18- year- old female foreign exchange student
named Jane. She has presented to your emergency department with severe
agitation, profuse sweating and hypertension. A few hours before admission,
she had been attending a rave party with her friends who were able to give only
a partial history for that evening due to their limited English. They are unable
to provide any previous medical or drug history. She is tachycardic at 140 bpm
with a BP of 180/100
mmHg and is hallucinating. Her core body temperature
is raised at 39 °C.
The Patient with a
Raised Temperature
What might be the cause of her clinical presentation?
Potential causes might include:
Drug poisoning (overdose or adverse eects)
Neuroleptic malignant syndrome
Serotonin syndrome
Sepsis
Intracerebral haemorrhage (e.g. aneurysm).
Given the history, what do you think is the most
likely diagnosis?
Jane is most likely suering from the toxic eects of recreational drug use. The
most likely ‘street’ drug she may have taken is ‘ecstasy’, a colloquial term used
to describe a group of illegal drugs. These include:
3,4- methylenedioxymethamphetamine (MDMA)
Gammahydroxybutyrate (GHB, also known as ‘liquid ecstasy’)
Benzylpiperazines.
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The Patient with a Raised Temperature
83
The concentration of MDMA is unregulated and inconsistent across for-
mulations so the exact ingredients may vary. This can expose individuals to
excessive doses. In addition, small doses may induce a toxic-
like reaction in
certain individuals who are unable to metabolise MDMA.
Which resources are available in the UK for information
and advice on acute intoxications and poisonings?
The National Poisons Information Service (NPIS) operates a 24- hour telephone
helpline, an online database (www.toxbase.org) and a mobile app, all of which
are very useful resources for clinicians treating patients with suspected/con-
rmed overdose.
What are the signs and symptoms usually
associated with the use of MDMA?
Given that the constituents of each formulation may dier along with their con-
centrations, dose- dependent clinical features may vary. MDMA is a derivative
of methamphetamine, which itself is derived from its parent compound
amphetamine. By increasing the net release of serotonin, noradrenaline and
to a lesser extent dopamine, the eects can be classied according to subjective,
physiological and adverse features:
Subjective eects
Euphoria and arousal
Extroversion
Enhanced self- awareness
Mental confusion and alterations to perception
Physiological eects
Tachycardia
Hypertension
Hyperthermia
Increased levels of prolactin and cortisol
Adverse eects
Nausea
Headache
Dry mouth
Agitation
Bruxism and trismus
What are the major patterns of clinical toxicity
associated with MDMA overdose?
There are four serious and potentially life- threatening patterns. These are not
necessarily mutually exclusive.
Hyperpyrexic type
The most dangerous form of toxicity. The hyperpyrexic adverse eects can
be exacerbated when taken at raves, due to increased physical exertion and a
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Clinical Cases in Critical Care
84
hot environment. Increased circulating noradrenaline causes vasoconstriction
which can lead to failure of redistribution of heat from the central circulation.
Severe cases may develop rhabdomyolysis, myoglobinuria and renal failure,
liver damage and disseminated intravascular coagulation. This type is the
leading cause of death in patients with MDMA overdose.
Hepatic failure
In mild cases, the hepatitis can often resemble a viral hepatitis with
spontaneous recovery occurring over weeks or months. In the most severe
cases, fulminant hepatic failure ensues. In the absence of a liver transplant,
this may prove fatal.
Cardiovascular toxicity
Release of noradrenaline can produce severe cardiovascular adverse eects,
most notably severe hypertension. This can lead to major intracranial haemor-
rhage, petechial and retinal haemorrhages, and tachycardia which can lead to
cardiac failure due to increasing cardiac workload.
Cerebral toxicity
Excessive uid intake and potential release of antidiuretic hormone (ADH)
can lead to the increased movement of water into tissues, including the brain.
Patients can develop epileptic-
type seizures and fatal compression of the brain-
stem and cerebellum.
What is serotonin syndrome?
Serotonin (5- HT) is a monoamine neurotransmitter that contributes to many
biological processes within the human body. In the presence of increased
release, reduced metabolism, reduced reuptake or stimulation of its receptors,
serotonin excess may produce a syndrome that includes:
CNS eects (e.g. agitation, confusion, delirium, coma)
Neuromuscular excitability (e.g. clonus, tremor, bruxism)
Autonomic instability (e.g. ushing, diarrhoea, tachycardia, hyperthermia).
Which factors may increase the risk of serotonin
syndrome?
This syndrome becomes more prevalent if the patient:
already takes prescription medications that increase or potentiate serotonin
levels, e.g. tricyclic antidepressants, selective serotonin reuptake inhibitors
and/or
consumes other stimulant recreational drugs in parallel, e.g. cocaine,
amphetamines, mephedrone.
While you are assessing Jane, the ED doctor tells you she has been considering
that this presentation could be caused by serotonin syndrome or neuroleptic
malignant syndrome in addition to the possibility of MDMA toxicity.
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The Patient with a Raised Temperature
85
What is the treatment for serotonin toxicity?
Benzodiazepines should be used as a rst- line treatment. These might include:
Oral or intravenous diazepam
Lorazepam
Midazolam (intramuscularly).
For severe overdoses with persistent hyperthermia, the use of cyprohepta-
dine (5-
HT
2A
antagonist) or chlorpromazine (5- HT
1
and 5- HT
2
antagonist) is
suggested.
What is neuroleptic malignant syndrome (NMS) and
how does it compare to serotonin syndrome?
Principally, NMS is associated with antipsychotic drugs such as chlorpromazine
or haloperidol. It may also occur with the newer drugs olanzapine, clozapine
and risperidone. It has a very low incidence amongst patients being treated
with these drugs (0.01–0.02%) and generally occurs during the rst 2
weeks of
treatment. It can also occur with chronic use. Increasing the dose of an anti-
psychotic rapidly and/or increasing its bioavailability (e.g. oral to intravenous
route) may also predispose a patient to NMS.
Its clinical features can mimic those of serotonin syndrome:
Hyperthermia
Altered mental status
Muscle rigidity
Autonomic instability (e.g. hypertension, tachycardia)
Raised creatine kinase levels
As with the serotonin syndrome, initial treatment consists of using benzodi-
azepines (as described above). However, in NMS, consideration could be given
to using dopamine agonists, such as bromocriptine or amantadine, following
discussion with the NPIS.
What is your initial management of Jane’s
hyperpyrexia?
Hyperpyrexia in this context is a potentially life- threatening feature which is
associated with disseminated intravascular coagulation and multiple organ
failure. Jane needs urgent cooling, utilising both passive and active methods.
You now measure Jane’s temperature to be 40 °C. She is increasingly agitated
and remains tachycardic and hypertensive. The ED team have already inserted
a peripheral intravenous cannula and sent blood samples for analysis of FBC,
U&E, LFTs, clotting and a group and screen. They have sent blood cultures,
requested paracetamol and salicylate levels and toxicology analysis of blood
and urine. Someone is attempting to obtain an arterial sample for blood gas
analysis, but it is proving challenging due to Jane’s agitation.
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Clinical Cases in Critical Care
86
Active cooling measures include cold uid lavage (e.g. bladder, gastric), ice
baths and administration of cold intravenous uids. Ice pads can be placed in
the groins and armpits and forced cold air blankets can be applied. Sedation
using diazepam should also be used when the temperature exceeds 38.5
°C,
and high doses may be required which may place the patient at risk if airway
reexes become suppressed. It can prove extremely challenging to reduce body
temperature to within the normal range.
What specic medication should you consider for
muscular hyperactivity in MDMA overdose?
Dantrolene–an initial dose between 2 and 3 mg/kg (maximum dose 10 mg/
kg) IV can be given. This markedly reduces the ability for muscle to contract
by reducing intracellular calcium. It is believed that dantrolene binds to
ryanodine receptor 1in the sarcoplasmic reticulum of skeletal muscle cells.
Which additional biochemical test should
you request and what might it demonstrate?
Serum creatine kinase–damage to skeletal muscle directly leads to elevated
levels of this enzyme in the bloodstream. Signicantly increased levels sug-
gest considerable muscle breakdown, with subsequent release of muscle
proteins such as myoglobin (which can cause myoglobin- associated renal
failure). If the initial level is normal but there is ongoing concern regarding
muscle damage then repeat measurements should be taken.
How could her hyperpyrexia be further managed?
The continued presence of hyperpyrexia increases the risk of mortality asso-
ciated with MDMA toxicity. It is imperative that her temperature is brought
down rapidly, and the next step would be to intubate, sedate and ventilate
Jane with complete muscle paralysis to reduce heat generated through muscle
contraction alongside the ongoing passive and active cooling interventions.
Sedating and invasively ventilating will also help facilitate other management
priorities, including obtaining a CT head to rule out an intracranial event, sta-
bilising her cardiovascular system, managing her gas exchange and correcting
any electrolyte disturbance.
What might be the cause of her low serum sodium?
One might assume that hypernatraemia would be more likely due to large
insensible losses secondary to increased environmental temperature and
muscle activity through energetic dancing. However, individuals consume
Jane has been in the emergency department for 30 minutes now. Despite
the active and passive cooling measures that have been used so far, her core
body temperature remains elevated above 38.5
°C.
The laboratory calls you to say that Jane's serum sodium is 115 mmol/L.
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The Patient with a Raised Temperature
87
alarge amount of uid to combat dehydration, resulting in a dilutional hypo-
natraemic state. In addition, as described previously, increased release of anti-
diuretic hormone may also play a part.
When does rhabdomyolysis occur?
Rhabdomyolysis occurs when there is damage to muscle cells that leads to
necrosis and the release of large amounts of intracellular solutes (e.g. potassium,
uric acid, lactic acid and myoglobin). It has myriad causes, which include
trauma, medications (e.g. statins, antimalarials), toxins (e.g. MDMA, cocaine,
snake venom), hyperthermia, ischaemia, electrical injury and infection. Its
main sequelae are acute kidney injury and potentially life-
threatening meta-
bolic abnormalities. The level at which a raised creatine kinase is suggestive
of rhabdomyolysis is generally accepted to be around 5000
U/L, but it should
be noted that myoglobin- induced renal failure can still occur below this level
if other predisposing factors are present (e.g. sepsis, hypovolaemia). Jane’s
serum CK is 20
000 U/L and she should be managed as having rhabdomyolysis.
Describe the Kidney Disease Improving Global
Outcomes (KDIGO) staging of AKI
KDIGO separates AKI into three stages (Table6.1).
How does rhabdomyolysis cause acute
kidney injury?
Free radical toxicity–most myoglobin that is released is normally bound
to haptoglobin. However, when the level of myoglobin increases beyond
the capacity for this buering action to take place, as in rhabdomyolysis,
the free myoglobin passes into the glomerular ltrate and causes damage
to the renal tubular cells through overproduction of oxygen free radicals.
This damage involves lipid peroxidation of fatty acids and polymerisation
of protein and DNA by malondialdehyde.
Renal vasoconstriction–the movement of uid into the damaged muscle
cells leads to a hypovolaemic state and therefore reduced renal blood
ow, which is exacerbated further by extraneous losses (e.g. profuse
sweating without increasing oral intake) and activation of the renin-
aldosterone- angiotensin pathway. Additionally, it is also proposed that
the ability of myoglobin to scavenge nitric oxide and release cytokines
may also play a part in the observed renal vasoconstriction.
You intubate Jane and initiate mechanical ventilation. Her temperature
begins to decrease below 38
°C and she appears to be stabilising physio-
logically. Her BP is now 120/70
mmHg and heart rate 100 bpm. CT brain
is unremarkable. You safely transfer her to your ICU following discussion
with your consultant. Her serum creatine kinase is found to be elevated at
20000 U/L. Serum creatinine is 200 μmol/L, and over the past 2 hours her
urine output has been consistently less than 0.5
mL/kg/h.
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Clinical Cases in Critical Care
88
Intratubular casts–the precipitation of myoglobin with Tamm–Horsfall
protein creates intratubular casts. This is accelerated in the presence of a
low pH (some practitioners induce an alkaline diuresis in these patients
for this reason).
How would you manage the rhabdomyolysis that
has occurred?
Early and aggressive uid resuscitation–restoring renal perfusion and
thereby increasing urine output are of paramount importance. Crystal-
loid solutions are most commonly used. Consideration should be given
to the patient who presents with severe oliguria or anuria as they may be
at risk of developing pulmonary oedema with rapid uid resuscitation
(particularly if a signicant cardiac history is present).
Bicarbonate therapy–the theoretical advantage of urine alkalinisation
in reducing the formation of casts has led to the use of intravenous
8.4% bicarbonate to increase the urine pH above 7.5. However, there
is no strong evidence from randomised controlled trials to support its
use. Ideally, since the drug is highly irritant to veins and can cause local
necrosis from extravasation, it should be administered via a central intra-
venous catheter.
Renal replacement therapy (RRT)–it is important to remember that
starting RRT should not be guided by the creatine kinase level but instead
by the status of renal impairment. In addition, as myoglobin has a molec-
ular mass of 17 kDa, it may be poorly removed using conventional tech-
niques. However, in critical care, the use of continuous venovenous
haemoltration (CVVH) is common and is eective at removing myo-
globin from the circulation in most cases.
Mannitol–this osmotic agent can eectively decrease uid within the
damaged muscle, prevent cast formation and increase renal blood ow
and glomerular ltration. However, in patients with post- traumatic rhab-
domyolysis and creatine kinase levels >5000 U/L, the use of mannitol
does not prevent renal failure or the need for renal replacement therapy
or decrease mortality.
Table 6.1: KDIGO classication for acute kidney injury.
Stage Serum creatinine Urine output
1 1.5–1.9
× baseline or 26.5 μmol/L increase <0.5 mL/kg/h for 6–12 h
2 2.0–2.9
× baseline <0.5 mL/kg/h for 12 h
3 3.0
× baseline
or
Increase in serum creatinine to
353.6 μmol/L or
Initiation of renal replacement therapy or
In patients <18 yr, decrease in estimated
glomerular ltration rate to <35
mL/min
per 1.73
m
2
<0.3 mL/kg/h for 24 h
or
Anuria for
12 h
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