Download S Naidoo (Deliberate Self Harm in the ICU)

20 April 2012
No. 13
Deliberate self harm in the ICU
S Naidoo
Commentator : Y Mzoneli
Moderator: J Taylor
Department of Anaesthetics
CONTENTS
GENERAL COMMENTS ........................................................................................... 3
KING EDWARD ICU STATISTICS ........................................................................... 6
OVERVIEW OF DIFFERENT METHODOLOGIES OF SUICIDE AND THEIR
CLASSIFICATIONS ................................................................................................ 10
THE PROBLEM ...................................................................................................... 11
CLINICAL PRESENTATIONS OF COMMON METHODS OF DSH TO ICU ........... 12
SPECIFIC AGENTS/METHODS AND MANAGEMENT .......................................... 13
Paracetamol ........................................................................................................ 13
Salicylates ........................................................................................................... 14
Tricyclic Anti-Depressants (TCAS) ................................................................... 15
Ketamine (Vitamin K,Jet, Special K) ................................................................. 17
Opioids/Narcotics ............................................................................................... 18
Anti-Epileptics .................................................................................................... 19
Herbal Agents ..................................................................................................... 20
Asphyxiations ..................................................................................................... 21
Drowning ............................................................................................................. 22
Trauma ................................................................................................................ 22
Caustic Ingestion................................................................................................ 23
Burns ................................................................................................................... 25
AN APPROACH TO DSH ....................................................................................... 28
CONCLUSION ........................................................................................................ 32
REFERENCES........................................................................................................ 33
Page 2 of 35
GENERAL COMMENTS
In a brief overview of the subject of Deliberate Self Harm (DSH) otherwise commonly
referred to as ‘suicide’, our discussion will focus more on the management of the
clinical presentations and complications of the various methods in an ICU setting.
However, this discussion will not be complete without a brief overview of the
psychology behind these victims. Suicide is a well know phenomenon dating back to
biblical times.
In nature we get teary eyed with the legend of the ‘thorn bird’ that commits suicide as
a last great act love, too bad we can't get to ventilate the bird so that it can give us a
repeat performance. However DSH has much more ominous implications in the
critical care environment.
The problem is becoming even more complicated as the age of patients are no
longer within any particular range, from love scorned teenagers or fanatical suicide
bombers to geriatric victims of dementia or bankruptcy.
The spectrum of the different methods of suicide is becoming even more ingenious
depending on the level of desperation or intelligence, the facilities at hand and the
statement the victim is intending to make.
Along with the variation of techniques, we are also being faced with a wide variation
in clinical presentations as well, from toxin induced organ failure to trauma induced
organ destruction.
In South Africa, we are presented with another unique angle to this problem from a
healthcare perspective and that is the availability of traditional or herbal medication.
The confounder in this situation is our lack of knowledge of the ingredients in the
concoctions that they supply to their victims and we are faced with difficulty in both
diagnosing and in treating the presenting features of these toxic traditional
ingestions, whether intentional or accidental.
Due to the complicated nature of these pathologies, the ICU stay is usually
unpredictable and complicated as the pathology evolves in its presentation and most
times the diagnosis is only made post-mortem.
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The other problem in treating suicide victims is that resuscitating them does not
necessarily save their lives. Serious suicide victims have to undergo rigorous
psychological assessment, counselling and monitoring in order to avoid repeated
attempts many of which are statistically successful. (4)
Therefore, for all intents and purposes, the management of victims of suicide or
attempted suicide should be a team effort encompassing the skills of the physician,
intensivist, psychologist, law enforcement or legal system and the family.
DSH has been categorised by psychiatrists into suicide (those that seriously attempt
to and succeed) and para-suicide (those that attempt to and don’t succeed for
whatever reason, i.e. no courage to go through with the deed or just looking for
attention. (4)
Within both of the above categories, clinicians are presented with a spectrum of
pathological characters or complications depending on the techniques used and their
associated management dilemmas (Table 1).
For the unfortunate candidates, the ultimate outcomes are sometimes determined by
unanticipated sequelae of hospitalisation instead of the suicidal attempt per se. By
the same token of misfortune, the victims may also deal with tragic lifelong
consequences of their actions, like physical scarring, cognitive impairment,
employment issues, domestic disintegration and social stigmata.(5)
Some suicide attempts are the result of ingenious contraptions by highly intelligent
individuals which cause injuries and pathologies that makes diagnosing and
managing these patients a challenge. In terms of deliberate self-harm we would like
to think that it is actually the unfortunate few that reach medical attention.
Page 4 of 35
Table 1. Popular methods of DSH
Chemical
Physical
Poisons - off the shelf
Gunshots
Prescription Drugs
Asphyxiation
Illicit drugs
Drownings
Industrial chemicals
Jumping from heights
House-hold chemicals
Vehicle related – driver
Herbal medication
Vehicle related – pedestrian
Slitting wrists/throat
Burns
Animal bites and attacks
By Proxy – suicide on order
Inhalation – Carbon monoxide/gas
In these categories, we find a spectrum of problems that present in hospital:-
Serious attempts that survive
Attention-seeking
complicate
Page 5 of 35
attempts
that
The cost to health-care in most instances are exorbitant and at times, ongoing. Some
would argue that these resources could have been better spent. Unfortunately
government legislation and ethics precludes us from taking on the management
decision ourselves.
Carrigan and Lynch, back in 2003 stated that:The incidence of suicide surpasses homicide and is the eighth leading cause of
death in the United States. About 1% of total deaths are a result of suicide.
Unsuccessful attempts outnumber completed suicides by a multiple of 16:1. (6)
By this, they mean that more people ended up in hospital than in the mortuary. The
male/female demographics of this problem can also be classified and quantified as
the problem becomes more rife and popular among all age and societal groups.
KING EDWARD ICU STATISTICS
The analysis of patients admitted for the period Feb 2011 up to and including Feb
2012. These numbers do not include requests for bed that were regarded as not
needed / futile or died before arrival to the unit.
These are numbers for the period of one year in one unit in one of about 76
provincial hospitals in one of 9 provinces. The number of DSH patients NOT
indicated in these reviews is unimaginable and therefore the true extent of this
problem is humongous.
The other derivation from this review is the means of suicide.
In this list we only encounter a few benign methods in which these patients survive.
The real McCoy’ is actually in the methods found in patients lying in mortuaries.
Page 6 of 35
Table 2. KEH ICU Stats
Age
23
34
23
17
29
16
14
15
35
33
48
22
47
35
22
39
35
27
63
14
22
37
Key:
M
F
B
W
I
OD
AED
D/C
RIP
Sex
F
M
F
M
F
F
M
F
F
M
M
M
M
F
F
F
M
M
M
M
M
M
Race
B
I
I
I
B
B
B
B
B
B
I
B
B
B
I
W
I
B
B
B
B
W
Method
Ingestion - ?herbal
OD
OD – AED
OD - ?
OD – Paracetamol
OD – Ethylene glycol
OD - ?
OD – Upper GIT bleed
Herbal intoxication
Herbal Intoxication
OD - ?
OD – Paracetamol
Organophosphate
OD
Anti-freeze
OD
Brake-fluid
Brake-fluid
Herbal ingestion
OD
OD - Paracetamol
Para-suicide
Male
Female
Black
White
Indian
Overdose
Anti- epileptics
Discharge
Dead
Page 7 of 35
Stay
5
6
5
4
10
2
2
29
8
4
4
1
3
3
7
2
4
14
7
7
3
3
Outcome
D/C
D/C
D/C
D/C
D/C
D/C
D/C
D/C
D/C
RIP
D/C
D/C
D/C
D/C
D/C
D/C
D/C
RIP
RIP
D/C
D/C
D/C
Table 3. Method analysis
Method
Number
Prescription Drugs
40%
Herbal Medication
30%
Domestic Chemicals
5%
Other
25%
NB: This is a 1 year examination of patients that presented to the unit with an
obvious diagnosis of attempted suicide. This does not include patients that were
treated for other related emergencies and sent out dead or alive without the true
aetiology being determined, it does not include patients that were accepted that did
not survive to be transferred across, nor does it include victims that were assessed
and deemed not fit for ICU management and it does not reflect victims that never
made it to our facility or any other facility for that matter i.e. they succeeded in their
objectives the first time.
So in summary, it is not a comprehensive indication of the general population stats
or even the regions. However, it is an indicator of the existence of the problem and
a taste of the potential cost of this activity to the health budget.
The demographics of suicide or para-suicide roughly follows particular social and
ethnic patterns. High earners tend to use more sophisticated methods and do so for
more financial reasons while middle and low income earners tend to have more
psycho-social issues that trigger them. (NB: ANYBODY does it for ‘love’). The
male/female choice of methods generally indicate that males tend to use more
violent means and females tend towards less bloody/traumatic forms of DSH.
Firearms, suffocation, and poison are by far the most common methods of suicide
overall. However, men and women differ in method used to commit suicide:
- Males: firearms (56%); suffocation (23 %); poisoning (13 %)
Females: firearms (31%); suffocation (19 %); poisoning (40%)(9)
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In broad categories, we can define 3 distinct groups of suicidal mechanisms:-
Within these categories, we can associate almost every possible way patients have
presented themselves either dead or alive as a result of DSH.
Ingestions: Drugs
 Chemicals
 Toxins
Asphyxiations: Strangulations
 Hanging
 Drowning
 Smothering
 Gassing
 Choking
Violence/Trauma: Falls
 Motor vehicles
 Gunshots
 Stabbing/ slitting
 Explosions
 Burning
 Electrocution
Page 9 of 35
OVERVIEW OF DIFFERENT METHODOLOGIES OF SUICIDE AND THEIR
CLASSIFICATIONS
Page 10 of 35
THE PROBLEM
The internet, the media and public access to weapons, drugs, chemicals and high
pressure lifestyle all contribute to the increasing rate of suicide attempts as well as
the growing complexity in treating survivors. Copycat victims, taking instruction from
media exposure of these activities or internet fundis that research it first on the web,
fall into two categories:a) Those that do it successfully and achieve their objectives
b) Those that do it incorrectly and survive (and at most times end up in our care).
All suicide attempts can be put into these categories and the implications of the
medical management to medical facilities are unique to each type. Their
management, their complexities, their consequences and their cost to health-care
are dependent on the methods chosen and the condition of the survivors.
Other factors that impact on the type of patient presenting to our care:- The co-morbid state of the victims, those with significant illnesses, has a
greater chance of succumbing to a complication of hospitalisation rather than a
complication of the suicide attempt.
- Sex - males tend to choose more violent methods (9) and survivors usually are
in a worse clinical condition at presentation. Females, however will be less
dramatic, and tend to choose methods that are painless and quick and less
conspicuous. So the survivors that reach medical attention may be more
surgical or more medical respectively.
- Socio-economic circumstances – lower income groups will tend to use more
common methods that are at their disposal. We are usually presented with
caustic or toxic ingestions that have a long protracted recovery and significant
co-morbidities. (9)
- Traditions and beliefs – the access to traditional healers and superstitions
about the after-life sometimes influence the choice of methods of suicide such
as techniques that cause outcomes that may be regarded as taboo. For
example, cults are known to commit mass suicides and select methods that
are pain-free, quick and palatable to mass victims including children, like
poisonings. In some cultures it is regarded as an honourable and acceptable
death to set oneself alight at a funeral of a departed spouse.
- Political or religious motivations – most of these candidates select methods
that will make a ‘statement’, the consequence of that can be ‘collateral
damage’ and the bigger the damage, the louder the statement. For example, a
suicide car bomber will again present with mass casualties and a significant
utilisation and drain of resources. (10)
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CLINICAL PRESENTATIONS OF COMMON METHODS OF DSH TO ICU
Airway
Patients that reach intensive care will come from either casualties or operating
theatres as a result of morbidity related to DSH. This does not exclude referrals from
acute medical emergency departments.
By inference, they will have some form of protected airway in place, intravenous
access and basic monitoring. The decision to insert a definitive airway will be
determined by the nature of the trauma and can range from a face mask to a surgical
airway. We must bear in mind that the need for airway security can change
depending on the clinical course. On the rare occasion, they may come in for
monitoring with a non-invasive airway device in place. Patients will be intubated for:I.
II.
III.
I.
II.
III.
IV.
V.
Airway protection – from caustic ingestion, chemical burns, smoke and fire
damage to URT, local trauma, anaphylactic reactions with soft tissue oedema,
low GCS and need for ventilation and aspiration risk.
Airway maintenance – upper body burns and oedema, trauma to upper
airways with gross soft tissue disruption and anaphylactic reactions
complicating the URT, metabolic derangements requiring ventilation.
Ventilation – severe acidosis, hypoxic ischaemic encephalopathy, major
trauma, toxin or trauma induced status epilepticus. (8) Breathing - rarely we
are presented with a spontaneously breathing patient on a face mask, CPAP
mask or intubated on a T-Piece. At most times however, due to the severity of
the metabolic or physiologicderangement or anatomical disruption, we have
patients that are in controlled modes of ventilation and may require deep
sedation. Depending on the source of their referral (from operating theatres
or from casualties) they may be ventilated for a variety of reasons: - (8)
Overwhelming respiratory or metabolic acidosis from shock, hypoxia, sepsis
or toxins
Significant cardio-respiratory trauma
Significant neurological trauma
Toxin induced muscle paralysis
In anticipation of organ donation
Page 12 of 35
Circulation
This presentation at ICU level usually implies that the patient is critically ill. Shock
with or without inotropic support is a common scenario. The management of shock
depends very much on the aetiology. The aetiology of shock can be overt or
concealed in an amalgam of systemic reactions to the harmful effects of some
chemical or trauma again, depending on the method of the suicide attempt:I. Toxin ingestion - early onset sepsis, anaphylactic reaction can stimulate an
intense inflammatory response that will put the patient into a circulatory shock
state- cardiogenic shock - that will require inotropic support.
II. Traumatic methods that result in major blood loss, even a slit wrist with radial
or ulnar arterial involvement can result in significant blood loss – hypovolemic
shock - that will require fluids, blood and inotropes.
III. Ingestions of drugs like slimming cocktails, thyroid supplements, and
serotonergic medication etc. Hyper dynamic picture and will require urgent
blood pressure management.
IV. Inflammatory reactions of certain medications, especially herbal concoctions
presents a toxic, hyperaemic, hyperthermic patient that will need aggressive
circulatory and metabolic control
SPECIFIC AGENTS/METHODS AND MANAGEMENT
We will focus on a few commonly presented examples of suicide related pathologies
and their progression. Due to the diversity of this subject, all methods of DSH cannot
be covered. However, in critical care and anaesthesia in general, we will be exposed
to these patients either for a procedure related reason or for management in an ICU
environment.
It is important that we understand the principals of management of this problem, the
changing need sometimes for urgent medical or surgical intervention, the times when
some interventions can be more harmful than beneficial, the times when the nature
of the condition warrants more counselling and palliation than heroic medical
expeditions and the times when medical management alone is not enough or even
necessary to save the patient’s life.
The following discussion will focus on popularly encountered methods that present to
ICU and will not follow any particular order.
Paracetamol
Toxic dose: - Adults 10g or 200mg/kg. An important consideration here is the delay
from ingestion to presentation: the earlier the presentation, the better the prognosis.
(11, 12)
Page 13 of 35
Presenting signs and symptoms: - Normally metabolised by the Cyp 450 pathway in
the liver. Glutathione conjugates the metabolites and excretes them via the
glucuronidation pathway. In toxic doses, this pathway is overwhelmed and toxic
metabolites accumulate, causing hepatocellular damage. Initially, the patient can
appear well. Over the next 1 – 2 hours, nausea and vomiting and right sub-costal
pain are indicators of toxicity.
Over the next 3 days, patients develop jaundice, coagulopathy, hypoglycaemia,
encephalopathy and liver failure with raise liver enzymes.
Management: a) Initial basic resuscitation – oxygen, IV access, fluids
b) If under 8 hours - Activated charcoal – 50g stat
c) Investigations: Paracetamol levels (assuming the agent is known or as part of
a toxic screen), baseline blood gases, blood sugar, clotting profile, liver and
renal functions and haematological indices.
d) N-Acetyl cysteine(NAC): 150 mg/kg NAC in 200 ml 5% dextrose over 15
minutes followed by 50 mg/kg NAC in 500 ml 5% dextrose over 4 hours
followed by 100 mg/kg NAC in 1000 ml 5% dextrose over 16 hours in adults.
e) Continued organ support and monitoring improvement or deterioration of
patient’s condition by assessing the above parameters.
f) Liver function can be further assessed by monitoring blood ammonia levels
Common outcome: Multiple factors determine outcomes
 Time of presentation
 Dose consumed
 Other components of the “suicide cocktail”
 Co morbidities of the patient
 The extent of organ dysfunction by the time of presentation
 The degree of recovery to pre-morbid level of organ function
Salicylates
Toxic dose:  150mg/kg - severe toxicity
 500mg/kg - lethal
Presenting signs and symptoms: - (14, 15) Toxicity begins with an initial stimulation of
the respiratory centre resulting in a respiratory alkalosis with compensating renal
HCO3, Na and K excretion. Hydrogen is exchanged in the kidneys for K resulting in
later metabolic acidosis.It results in the uncoupling of oxidative phosphorylation and
accumulation of pyruvate, lactate, sulphuric and phosphoric acids as well as a switch
to anaerobic metabolism.
Page 14 of 35
The end stage metabolic picture is a mixed metabolic alkalosis and acidosis and a
respiratory alkalosis, hypokalaemia, hypoglycaemia and dehydrated patient. The
patient presents with vomiting, tinnitus, confusion, seizures, hyperthermia, primary
respiratory alkalosis, primary metabolic acidosis, and multiple organ failure. The
CVS, respiratory, renal, hepatic and CNS are all involved in the organ dysfunction.
In children and elderly, they may present with non-cardiogenic pulmonary oedema
and/or acute lung injury and Reye’s syndrome (nausea, vomiting, elevated liver
enzymes, fatty infiltration and coma or death). Platelet and bleeding disorders and
acute fulminant hepatic failure can occur.
Management: Salicylate levels - directed or as part of toxic screen - therapeutic range : 15–
30 mg/dL
 Bloods – liver and renal function, clotting profile, glucose, blood gas,
 CXR, AXR, ECG - free air shadows and arrhythmias
 Empty the stomach – “it’s never too late to aspirate with salicylate” – gastric
lavage up to 12 to 24 hours post ingestion
 Activated charcoal 1 – 2 g/kg
 Symptomatic treatment and organ support – Ventilation, dialysis, sedation,
fluids – Ringers lactate or NaCl to support an alkaline diuresis. The theory is to
alkalinise the urine, to draw the Salicylic acid across, the so-called ‘ion trap’.
The goal is to increase the urinary pH to 7.5 by a NaHCO3 infusion. The
technique only works if the patient is normokalemic. Hypokalemia will cause
renal re-absorption of K+ in exchange for H+ resulting in acidic urine. Therefore,
monitor and supplement the potassium.
 Patients will need haemodialysis if serum level greater than 120 mg/dL
(acutely) or greater than 100 mg/dL (6 h post ingestion), refractory acidosis,
coma or seizures, no cardiogenic pulmonary oedema, volume overload, and
renal failure.(14,15)
Common outcome:As above but higher incidence of GIT and renal complications.
Tricyclic Anti-Depressants (TCAS)
Toxic dose: - Patients will commonly ingest a combination of TCAs in a cocktail form
or high dosages of a particular agent. Toxicity depends on the agents.
Presenting signs and symptoms: - TCAs increase the synaptic concentrations of
biogenic amines (adrenalin and noradrenalin) and indoleamines (serotonin and
histamine) by reducing their uptake. They also have significant anticholinergic and
anti-alpha2 receptor effects. Concentrations in heart, liver and neural tissue increase
much faster than in plasma.
Page 15 of 35
Cardio toxicity - presenting as PVCs, SVTs, VTs, re-entrant arrhythmias. Asystole
generally follows bradycardia and hypotension. TCA induced VT and VF are usually
refractory to treatment. (16)
Neuro-toxicity - hallucinations, confusion, seizures and coma are common. (16,17,18)
beside routine criteria, centres have developed specific criteria for admission to ICU
for these patients based on ECG changes (38). Based on studies done at the
University of Michigan and by Callahan et al, the algorithms identify patients that
have a higher risk of seizure and cardiac arrhythmic activity related to the length of
the QRS complex. QRS complexes > 0.10 seconds are ominous.
Management: The early establishment of a secure airway and initial basic resuscitation
should begin on presentation.
 A low threshold for activated charcoal protocol, and supportive treatment for
sequential organ dysfunction should be timeously initiated, i.e. respiratory
support to prevent hypoxic brain injury, renal support for kidney injury, hypoxia
or metabolic changes and cardio toxicity must be monitored and managed.
 First line drugs are Diazepam 2.5 – 5mg increments until seizures are under
control.
 Alkalosis is of benefit to these patients as it increases protein binding of these
drugs and removes them from plasma. NaHCO3 1mg/kg IVI or hyperventilation
is recommended.
 Atrio-ventricular conduction defects should be managed aggressively. These
patients are intractable to most therapeutic measures and a low threshold for
pacing must be entertained.
 VT responds quickly to Lignocaine 1mg/kg, repeat boluses may be needed.
 Fluids and inotropes should be considered for hypotension.
Common outcome:- variable, as above
Benzodiazepines (BDZ)
(Flunitrazepam, Diazepam, Midazolametc.) Commonly prescribed drugs for sedation,
anxiolysis and muscle relaxation.
Toxic dose:- Depends on the agents used. Reference ranges available from local
labs/poison centres.(19).
Presenting signs and symptoms:-Sedation with of loss of airway reflexes is a
common cause of fatality. By itself, it is uncommonly lethal but it is commonly coadministered with alcohol or other street drugs(19) and these combined effects result
in cardio-respiratory events.
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Management: Resuscitation on initial presentation.
 Has a direct antagonist –Flumazenil – potent BDZ receptor antagonist,
inhibiting the action at the BDZ/GABBA receptor - administered as soon as
presence of agent is confirmed. 0.2mg over 15 s, repeated as per response up
to 1mg over 20 min intervals (18)
Common outcome:- Relative to the associated effects of overdose i.e., hypoxia,
hypotension or effects of other ingredients of the cocktail.
Ketamine (Vitamin K,Jet, Special K)
Toxicity:- Commonly used as a general anaesthetic agent in this country but widely
used by drug abusers as a social drug for recreational purposes. It is snorted as a
powder, injected IVI / IMI, taken PR with a lubricant. (20)
Presenting signs and symptoms:- The main effects are cardiovascular and
neurological. Causes dissociative symptoms – (trip down the
‘K-hole’schizophrenia-like state), loss of reflexes, loss of consciousness, delirium, euphoria,
seizures, coma and death. It can result in a severe hypertensive reaction and CVS
overstimulation. Levels can be tested from almost any biological fluids.
Table 4. Organ specific Ketamine levels
Source
Lethal Level
Bile
1.3-15mg/L
Urine
1.2-8.5mg/L
Blood
1.5-38mg/L
Kidney
3.2-3.6mg/kg
Liver
4.9-6.6mg/kg
Brain
3.2-4.3mg/kg
Cardiac muscle
2.4mg/kg
Stomach contents
21mg/L
(Table taken from Forensic toxicology news and community website) Significant
renal, hepatic, cardiac and neurological dysfunction can occur. Chronic abusers
present with high dose toxicity due to tachyphylaxis after long term use. Organ levels
can be unbelievably high.
Page 17 of 35
Management: No specific antidote
 Mainly supportive care
 Sedation with benzodiazepines - seizure control
 Mechanical ventilation if indicated.
 Routine measures like activated charcoal, alkalinisation and dialysis may be
considered depending on route of administration, dose and time frames.
Outcome:Can be fatal if patient is not managed timeously. Cardiac arrest and encephalopathy
from hypoxia.
Opioids/Narcotics
Opioids range from prescription drugs like Morphine, pethidine, codeine to illicit
drugs like heroin. They work via depressing the CNS, and compromising respiratory
and autonomic functions. Opioids affect the CVS (33) – Fatal arrhythmias like
prolonged QT types. Respiratory effects include blunted response to hypoxia and
respiratory depression and hypercarbia by mu receptor induced blunting of
chemoreceptors in the brainstem.(21) The issue of ‘tolerance’ in chronic opioid users
and the problem of concomitant BDZ and alcohol abuse in these patients can
confuse the clinical picture. These patients will present to ICU for respiratory
depression related complications. Hypoxic brain damage has to be excluded based
on the history and clinical picture. Myocardial infarcts, heart failure and cardiac arrest
after ingestion are poor prognostic indicators. (21, 22, 23, 28)
Management:-Primarily organ support: Ventilation
 Inotropic support
 Dialysis if indicated
 Reversal of toxins if an agent is available. This is fortunately one of the few
drugs where a definite antidote is available – Naloxone is an opioid receptor
blocker that stops opioid agonists from activating them. Unfortunately, it also
reverses the analgesic and sedative effect of the opioids.
 Naloxone - 0.4 to 2 mg/dose IV/IM/subcutaneously. May repeat every 2 to 3
minutes as needed. Therapy may need to be reassessed if no response is
seen after a cumulative dose of 10 mg.
 Continuous infusion: 0.005 mg/kg loading dose followed by an infusion of
0.0025 mg/kg/hr.(Drugs.com site – online drug information site)
Hereafter the management is largely supportive until the patient recovers from the
impact of the dose on the organs.
Page 18 of 35
Anti-Epileptics
Common agents:Carbamazepine; Phenytoin; Lamotrigine; Topiramate
Presenting signs and symptoms:- Usually CNS related symptoms – drowsiness,
ataxia, nystagmus, dysarthria, dyskinesia, brainstem symptoms, ophthalmoplegia,
diplopia, opisthotonus and choreoathetosis.(23) CVS symptoms – arrhythmias, heart
blocks, QRS and QT segment changes.
Management:- Most times, treatment is symptomatic, organ support and time. On
the extreme, dialysis may be beneficial. Activated charcoal in patients with reduced
level of consciousness is controversial.
Common outcomes:- Dose, agent and cocktail combination determines the outcome.
Can be fatal.
Organophosphates
Toxic dose:- Regarded primarily as a toxin. Never normally meant for human
consumption, therefore any dose can elicit harmful/fatal symptoms.
Presenting signs and symptoms:- Predominant effect is inhibition of
anticholinesterase and symptom features described as a ‘cholinergic crisis’, with
autonomic, somatic and CNS symptoms. (24,26)
Clinical manifestations of acute organophosphate poisoning:Table 5.
Muscarinic
Nicotinic
Central nervous system
Diarrhoea
Urinary incontinence
Meiosis
Bradycardia
Bronchorrhoea
Bronchoconstriction
Salivation
Lacrimation
Emesis
Hypotension
Cardiac arrhythmias
Fasciculations
Altered
level
of
Tremors
consciousness
with
Muscle weakness with respiratory failure
respiratory failure
Seizures
Hypertension
*Atrial fibrillation, ventricular
Tachycardia
fibrillation and heart block
Sweating
have been
Mydriasis
*Table taken from Aardema. (24)
Secondary weakness of limbs and respiratory muscles also dominate the crisis.
Page 19 of 35
Management: The mainstay of treatment is anticholinergic agents.
 Atropine 3–10mg loading doses and 1–2 mg half hourly as maintenance until
symptoms resolve, or to a lesser extent glycopyrrolate, is used as a direct
antidote and dosage is titrated to effect.
 Other features are treated symptomatically viz. seizures, hypotension,
diarrhoea. It is not unusual to have these patients on full organ support for a
prolonged period of time until symptoms resolve and a large percentage of
these patients actually succumb to complications of critical care management.
Common outcome:- as above.
Herbal Agents
Agent:- Usually the cocktails are foreign to clinicians. Common agents with known
effects can be quickly managed but most times these patients are diagnosed post
mortem and even then it’s just ‘toxic ingestion’ as the final diagnosis with no clearly
identified agent stipulated. Attempts by authorities to regulate the spectrum of
agents available have failed due to the availability of informal practitioners that don’t
comply with any regulations or belong to any regulatory body. Therefore important
features of these agents like package labelling and advice on antidotes are not
necessarily mandatorily available to users as opposed to mainstream
pharmaceuticals. (25)
Toxic dose:- unknown
Presenting signs and symptoms:- The four commonest systems involved in fatal
herbal intoxications are the GIT, renal, neurological and haematological, although
NO system is entirely spared. Presentations of seizures, reduced levels of
consciousness, hallucinations, bleeding and intractable nausea and vomiting are not
uncommon. Other common symptoms are cardiac arrhythmias, respiratory failure,
renal failure, GIT symptoms, anaphylactic reactions and unexplained pneumonitis.
Hepatic symptoms can range from a mild hepatitis to fulminant fatal hepatic failure.
Lab results can be equally confusing with haematological, electrolyte and toxin
findings that can mimic common conditions or be completely unexplainable.
Management: Gastric lavage is for the majority of times contra-indicated as these
patients have a reduced level of consciousness or the nature of the agent
is unknown and aspiration risk outweighs the benefit.
 The use of activated charcoal has been recommended in the first 24
hours of presentation.
 Due to the lack of knowledge in this field and the absence of clear defined
antidotes we are again reduced to symptomatic and supportive treatment.
Common outcome:- variable but often fatal.
Page 20 of 35
Asphyxiations
Mechanisms:Intentional- Hanging, strangulation, any form of upper airway occlusion Accidental –
anaphylactic reaction
Presenting signs and symptoms:- Patients will present for either metabolic outcomes
of asphyxiation - hypoxia or for injuries related to the technique used.
Hanging - Constrictive force applied to the cervical region with the intention of cutting
of the supply of oxygen to the patient or rapid transection of the cervical spine with
complete loss of neuro-systemicl communication. If successfully done, can be an
efficient method of suicide or murder.
If it goes wrong, the complications can be catastrophic.(27) Death results from
constriction of the larynx or tracheal lumen, from loss of blood supply to the brain by
constriction of the carotids and/or from traumatic (27,37)rupture of the cervical
spine. In the event that the patient does not die, these are the areas of injury that
they will present with.
Then the mechanism of death will be from cerebral infarction, hypoxic
encephalopathy, pulmonary oedema, aspirations and infections. Survivors will suffer
the consequences of cerebral injury, pulmonary injuries and cognitive deficits. These
patients may present with overt signs of trauma and asphyxiation as described
above or concealed internal injuries to cricoid, hyoid bones, laryngeal cartilages,
vascular structures of the neck and neural structures of the spine. A thorough
examination of the patients head and neck region, skin changes/marks, voice
changes, changes in the tone and mechanism of breathing. After the initial
stabilisation and resuscitation, direct inspection by laryngoscopy and imaging must
be used to assess the extent of injury.
Management:o Anatomical stabilisation of the bony structures
o Securing the airway by intubation or surgically- extensive airway assessment
by rigid or fibre optic bronchoscopy is necessary to determine the extent of
damage and the limitations of intervention.
o Metabolic derangements
o Formal surgical airways and organ support are among the first line of critical
care management consideration. (37)
Strangulation and suffocation. Generally the presentations and clinical sequelae are
the same as in hanging, may be with less trauma depending on the method chosen.
Upper airway occlusion and hypoxia by any other means. As above.
Page 21 of 35
Drowning
This is a form of chemical asphyxia. Usually as a result of submersion of the head
and upper airways under water or any other liquid and the chemical is inhaled into
the air passages. Death occurs from one of 4 mechanisms:o Chemical pneumonitis - liquid entering the lungs
o Vaso-vagal cardiac arrest – impact of sudden cold water or pressure to
trunk
o Asphyxia – laryngospasm when liquid enters the larynx
o Post – immersion syndrome – infiltrative/exudative, infective
developments post resuscitation
Patients may present to health care with liquids in the air passages, oedema of the
air passages, hypoxic cardiac arrest, hypoxic brain injury.(28) Other presentations will
depend on the trauma related to entering the water, if it was clean or dirty water or
any other form of chemicals and their effects on the body.(28)
Management: Basic life supportive measures on presentation.
 Respiratory support, intubation and ventilation.
 Inotropes for cardiogenic shock.
 Early broad spectrum antibiotics for aspiration pneumonitis.
 Full body imaging if suspected that patient jumped from heights to exclude
other injuries.
 CXR for assessment of pulmonary state and monitoring progress.
Trauma
In suicide, this is a vast topic and can range from high velocity gunshot wounds to
the head or any other art of the body or to a patient jumping in front of a high speed
train. The spectrum of injuries can be an isolated long bone fracture to polytrauma
involving every system in the body.
Page 22 of 35
Management: These patients will present with the same spectrum of trauma related
complications as any other general trauma patients.
 Primary and secondary surveys will be done on presentation and ICU
admission will be meant for supportive management.
 Shock, large volume blood loss
 Sepsis, airway trauma, ventilation, loss of consciousness, cardiac and lung
contusions, etc. may all warrant ICU management.
 Admission stay to the unit can be long and complicated.
 Repeat OT transfers for fixation of fractures, exploration of abdomen, cleaning
of septic focuses and debridements, and recurrent infections results in
increasing morbidity and poorer long term prognosis.
 It is not unusual to have missed injuries detected later in the course of the
patients stay and can significantly affect the course in ICU.
 In these patients, even if the prognosis looks poor, aggressive resuscitation
and organ support may be prudent if organ donation is a consideration.
Caustic Ingestion
Agents can be acidic (pH < 7) or alkali (pH >7). Acids cause more of a coagulative
necrosis, this results in a layer forming on the mucosa that causes superficial
damage as the substance travels down into the stomach.
By implication, the damage is predominantly superficial on the upper oropharyngeal
tract. Alkalis however, form a liquifactive type of necrosis that penetrates quickly into
the deeper tissues.
Therefore the nature of alkali injuries is much more locally destructive. Mucosal
sloughing, collagen deposition and scarring are significant later sequelae that
determine the eventual outcomes of these patients. The nature of the substance will
determine the location of the destruction.
Liquids flow deeper into the mouth and oesophagus and damage deeper structures
like the oesophagus and stomach. Solids tend to adhere to the mouth and
oropharynx and cause local damage there.(30)
Symptom presentation will also give a likely clue to the type and location of the
injury, e.g. hoarseness and stridor – oropharynx; dysphagia, hematemesis and pain oesophagus and stomach
Page 23 of 35
Management: Resuscitation, assessment of the damage by imaging and direct visualisation
is paramount in the acute phase.
 Endoscopic grading of the burns is important in guiding management and for
prognostic reasons.
 However, it must be noted that the safe window for endoscopic examination of
these patients is within the first 12 hours and after 2 weeks. Tissue
inflammation, softening and necrosis outside this period can result in iatrogenic
injuries.(30)
Table 6 – Caustic injury grading(39)
First degree(superficial)
no ulcerative oesophagitis, mild erythema, oedema of mucosa
Second degree(trans mucosal)
whitish exudate, erythema, underlying ulceration that may extend into
the muscularis
Third degree(trans mural)
dusky or blackened trans mural tissue, deep ulcerations (may extend
into peri-oesophageal tissue, lumen may be obliterated)
Stricture formation is the most important long term consideration.
Table 7 – Prognosis(40)
Grade I = no oesophageal stricture risk
Grade II = 75% will develop stricture
Grade III = 100% will develop stricture
Some authors advocate the early use of steroids to prevent this. Prednisolone 1 –
2.5 mg in the acute phase and for up to 3 weeks has been shown to be protective.
Antibiotic use is dependent on the centre's protocols. On the whole, most centres
advocate using them only when evidence of secondary infection appears. The utility
of this grading system is evident in guiding feeding protocols and steroid use. Refer
to table 8 below: (34)
Page 24 of 35
Table 8. Prevention of Strictures – steroid recommendation
Grade 1: not necessary
Grade 2: most effective
Grade 3: surgery, risk of perforation
Dosage: controversial - recommendation: 1-2 mg/kg/day, 3weeks
Table 9. Feeding post injury
Oral Intake
- permit oral intake and discharged within days
- nutritional support by parenteral or NG tube (blind
passage increases risk of iatrogenic oesophageal perforation)
- NPO 3-5 days
- NPO >one week
ICU admission is warranted in the event of complications like aspiration, shock,
chemical pneumonitis, LOC, bleeding, upper airway obstruction and for support in
the event of the development of organ dysfunction: –
o Respiratory failure – ventilation
o Renal failure – dialysis
o Cardiac failure - inotropic support
o DIC
o SIRS and septic shock.
Response and has to be prompt and aggressive in these patients. Surgery for
dilatation, stenting and repair will also need ICU cover in sick or unstable patients.
Burns
Agent:- The spectrum of burns in these patients is no different from general burns
patients. They range from dry fire, electrical, chemical, boiling water, explosive
burns. They range from first degree to full thickness and inhalation burns. Sometimes
on presentation the only evidence of thermal injury is singeing of nasal hair or the
presence of soot in the air passages. (1, 2, 31, 35)
Page 25 of 35
Management: The mainstay of care in these patients is analgesia, fluids and organ support.
 Careful consideration has to be paid to co-morbidities, age and body surface
variations in these patients in view of the fact that of all DSH patients, these
variables affect both the degree of injury and the extensiveness of intervention
the most.
 In inhalation injuries (35) damage to the lung parenchyma is not the direct result
of heat but rather the presence of products of combustion, like debris and
oxides of sulphur and nitrogen, carbon monoxides and hydrochloric acids.
 A foreign body response is triggered by the debris.
 The bulk of the damage to lungs during burn injuries is as a result of pulmonary
oedema and consequent de-epithelialisation. This leads to a cascade effect,
obstructing and damaging the airways. The reduction in compliance due to
oedema formation, increase in extravascular lung water and pulmonary lymph
flow presents with ventilation difficulties.
 Atelectasis and areas of collapse due to inhibition of surfactant production
results in shunts and eventually a full ARDS picture.
 The key to getting ahead of the pathophysiology of this process is early
diagnosis and treatment.
 Some centres are already using fancy methods of assessment and diagnosis
like fibre optic bronchoscopy, Xenon scans and measurement of extra-vascular
lung water to distinguish parenchymal from upper airway injury.
 A further consequence of burn injuries is carbon monoxide poisoning and
further confounds the pathology.
 Early management of burns patients depends on a high degree of suspicion.
Once the diagnosis is confirmed, airway, fluid and analgesia should be
immediately managed.
 These patients regularly require early ventilation and aggressive antibiotic
treatment.
 Hypovolemic shock as a result of intravascular losses to the extravascular
compartment should be managed with inotropes.
 Other adjuncts like anti-coagulation, anti-inflammatories, physiotherapy and
early ambulation.
 These patients have significant long term sequelae, like tracheal stenosis,
parenchymal lung disease and cosmetic deformities.
 Full thickness burns will also require repeat aggressive debridement and
eventually skin grafting that will mean optimisation of the patient before
surgery.
 These patients can be a significant drain on resources of a regular ICU and
therefore early transfer to a dedicated burns unit is the gold standard of
management
Page 26 of 35
In summary, the management of DSH burns patients is the same as any burns
patients: Resuscitation – lines/fluids/oxygen
 Analgesia
 Surgery – debridements/escharotomies/airway
 Organ support as indicated – ventilation/Dialysis
 Investigations – Bloods, X-rays/Bronchoscopies
 Antibiotics – as required
 Adjuncts:






Adrenalin/bronchodilator nebs
N-acetyle cysteine - mucolytic
Anti-coagulation - Heparins
Physiotherapy
Ambulation
Pulmonary function testing, management and optimization
NB: In electrical and blast burns – CVS/CNS and GIT assessment is indicated to
exclude systemic injuries.
Common outcome:- Outcomes can be debilitating and further aggravate the
emotional state of the patient.
Toxidromes
Years of experience with the phenomenon of toxic ingestions have resulted in
clinicians developing customised terminologies that are unique to it. One such term
that we should get acquainted with is that of ‘toxidrome’. This is a syndromic
collection of symptoms, signs and features that together with the history should alert
the clinician of the possibility of toxin ingestion. (32) For example: Salivation, lacrimation, panic and anxious, GIT and urinary symptoms,
respiratory and cardiac
symptoms commonly indicate an Anti-cholinergic
Toxidrome. The features referred to in familiar circles as the patient being ‘Hot
as a Hare, Dry as a Bone, Mad as a Hatter, Red as a Beet and Blind as a Bat’.
 Disorientation, hallucinations, seizures, tachycardia, tachypnoea and
hypertension, point to an Amphetamine, Cocaine, Phencyclidine Toxidrome.
 Stupor, coma, disorientation, speech slurring and reduced level of
consciousness indicate a sedative, alcohol , BDZ Toxidrome.
 Altered mental state, stupor, hypopnoea, hypothermia and meiosis indicate an
Opioid Toxidrome
 Irritability, flushing, diarrhoea, fever, increased reflexes, tremors are strongly
suspicious of a Serotonergic Toxidrome.
Page 27 of 35
AN APPROACH TO DSH
The initial evaluation of these patients can be difficult in that ICU is a unique
environment. (6, 7, 8, 9)
DSH management Flow Diagram (6)
A number of features on history will indicate the seriousness of the attempt and give
an indication of the mental state of the patient.
Page 28 of 35
Table 10.
(Carrigan and Lynch et al) (6)
Outside of these criteria, the next related group of patients will be those that don’t
really want to commit suicide but accidently end up in need of critical care (i.e. the
attention seekers that miscalculate).
A generic approach is possible once it is ascertained that this patient is a victim of an
attempted suicide. (6,32)
History:  Drug/alcohol ingestion/addiction
 Personality disorders
 Evidence of materials and means
 Scars/marks/odours
Examination: Circumstantial evidence - bottles/syringes/odours/marks/scars/notes
(36)






Airway and respiration- obstruction/quality/secretions/saturation
Cardiac – Rate/Rhythm
Circulation – pressure/volume
CNS – mental state/LOC/seizure activity/paralysis/trauma
Renal – Function
GIT – Nausea/vomiting/bleeding/trauma/burns
Page 29 of 35
Special investigation: Routine bloods, incl. blood gas – anion gap
 Electrolytes – liver, renal functions, K+, Mg,Ca
 Toxicology screen – blood and urine - salicylates/paracetamol/antiepileptics/illicit drugs – ‘Rapid tests’ are available for quick bedside
diagnosis and early intervention.
 ECG – Cardiotoxicity/electrolytes abnormalities
 CXR – caustic ingestion – free air signs
 Endoscopy – ingestions
 CT/MRI scans for trauma or injuries.
Management:Principles:–
Traumatic – resuscitation and stabilisation
Ingestions – reduce absorption and speed up excretion
The decision to manage the patient in ICU has to be taken early and based on firm
diagnostic criteria. Some of the parameters identified by Brett et al (7) that need to
be considered are: PaCo2 > 45 mmHg
 The need for intubation and ventilation
 Seizures
 Arrhythmias
 QRS > 0.12s
 Shock – SBP < 80mmHg
 Second/third degree AV block
 Low GCS




Initial resuscitation/intubation/cannulation
If trauma then surgical intervention
Blood and urine analysis for drugs and toxins and baselines.
Stomach clearance of toxin ingestion can be achieved in 3 ways:
– Emesis – Ipecac +/- 30ml in adults PO – NB: aspiration risk.
– Gastric lavage – water based solutions, more benign and less likely to
contribute to the electrolyte derangements - wide bore nasogastric tube
– Activated charcoal 25 -50 mg to start and dose to be repeated as many
times as necessary to titrate to the response of the patient.
– Cathartics – glycerol is commonly used but evidence for this method of
detoxification is weak.
Page 30 of 35
 Some units – Coma cocktail (7) – Thiamine 1000mg, Dextrose 50g ivi or a 5%
DW, Naloxone 0.2 – 0.4 mg ivi and Flumazenil 0.2mg as a part of the initial
resuscitation.
 Organ support as indicated by clinical parameters that warranted theICU
admission.

Ventilation

Inotropic support

Fluids

Antibiotics

Blood transfusion
 Antidotes – refere table 11.
Table 11. List of known Antidotes (32)
Acetaminophen
Anti-cholinergics
Benzodiazepenes
Ca channel blockers
Carbamate
Cyanide
Digoxin
INAH
Methanol
Glycol
Opioid
Oral hypoglycaemics
Organophosphate
Warfarin
N-acetyl cysteine
Physostigmine
Flumazenil
Glucagon, Insulin + dextrose, Calcium
Atropine
Thiosulphate, nitrate
Digoxin antibodies
Pyridoxine
Ethanol, Fomepizole
Ethanol, Fomepizole
Naloxone
Glucose
Atropine,? P2AM
Vitamin K
Iron
Copper
Lead
Mercury
Arsenic
Antimony
Desferroxamine
Penicillamine, Dimercaprol, CaEDTA
CaEDTA, Dimercaprol (BAL)
DMPS, DMSA, BAL
BAL & derivatives
BAL & derivatives
 Extra-corporeal methods of toxin removal –
o Haemodialysis – for low molecular weight, water soluble, low protein
bound toxins, added benefit of metabolic correction as well.
o Hemofiltration – removal by convective currents, as blood flows through
highly porous material and large molecular weight toxins get filtered out.
o Haemoperfusion – blood in contact with an absorptive surface e.g.
Charcoal. Weight, solubility and protein binding is not an issue.
o Refere table 12 for list of dialyzable toxins.
Page 31 of 35
Table 12 – dialyzable poisons (41)
 Endoscopic investigation and intervention(debridement or stenting) –
Gastroscope/ Bronchoscope
 ICU protocols for continuous screening and adjustment of treatment until
patient stabilises and is no more in a life or limb threatening situation.
 Unlike accidental trauma, where the nature of the injuring agent is a threat to
the patient, in these cases, the patient is more of a threat to themselves and as
such, early liaisons with the family, other medical care givers and a
psychologist will speed up discharge from the unit.(6,7,8,9)
CONCLUSION
The DSH patient can raise serious ethical and moral dilemmas in the minds of
medical professional. It is however difficult to determine the state of mind of these
individuals that prompts them to go to these extremes. Despite the cost and
complications associated with this patient group, we treat them as any other patient
and manage them with all available resources.
Page 32 of 35
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