Thanks for requesting me to answer this question.
1) "Is it recommended to put patients who have suffered severe
head trauma into drug induced comas?"
Drug induced comas are most likely done by barbituates. From
Principal Health News:
"A barbiturate-induced coma, or barb coma, is a temporary state of
unconsciousness brought on by a controlled dose of a barbiturate drug,
usually pentobarbital or thiopental.
Barbiturate comas are used to protect the brain during major brain
surgery, such as the removal of arteriovenous malformations or
aneurysms. Coma may also be induced to control intracranial
hypertension caused by brain injury.
Barbiturates reduce the metabolic rate of brain tissue, as well as the
cerebral blood flow. With these reductions, the blood vessels in the
brain narrow, decreasing the amount of swelling in the brain. With the
swelling relieved, the pressure decreases and some or all brain damage
may be averted.
Controversy exists, however, over the benefits of using barbiturates
to control intracranial hypertension. Some studies have shown that
barbiturate-induced coma can reduce intracranial hypertension but does
not necessarily prevent brain damage. Furthermore, the reduction in
intracranial hypertension may not be sustained."
Here are the indication for a barbituate-induced coma trom Trauma.org:
"Brain damage resulting from head injury is the leading cause of death
among individuals younger than 24 years of age. The most hazardous is
increased ICP. High-dose barbiturates are used to control intracranial
hypertension in selected patients. ICP is decreased due to decrease in
CBV due to vasoconstriction caused by increase in cerebrovascular
- Potentially survivable head injury
- No surgically treatable lesion accounting for intracranial
hypertension (except when used for preparation for surgery)
- Other conventional therapies of controlling ICP have failed
(posture, hyperventilation, osmotic and tubular diuretics,
- ICP > 20 to 25 mmHg for more than 20 min, or >40 mmHg at any time
- Unilateral cerebral hemispheric edema with significant (>.7 mm)
shift of midline structures shown on CT
- A low Glasgow Coma score"
Dr. Wetzel of the Children's Hospital in Los Angeles recommends
barbituate-induced coma in the following cases:
"Barbiturate-induced coma should be considered if intracranial
pressure is not controlled by a combination of:
- temperature regulation
eMedicine.com suggests using barbituate-induced coma when all
conventional therapies have failed on controlling increased
"Barbiturate therapy lowers the ICP and exerts cerebral protection
through several mechanisms: alterations in vascular tone, inhibition
of free radical mediated lipid peroxidation, and suppression of
metabolism. By lowering the metabolic demands, it decreases the
cerebral blood flow and related cerebral blood volume providing
beneficial effects on the ICP and global cerebral perfusion. However
several studies have shown that barbiturate therapy does not improve
outcome when compared to mannitol, empiric coma therapy or when used
as prophylactic treatment of ICP.
The only patients to respond favorably to barbiturate ICP control seem
to be those in which the cerebrovascular autoregulatory response is
preserved. Therefore their use should be reserved only for intractable
increased ICP when all conventional medical therapies have failed. The
goal of barbiturate therapy should be directed to achieve
electroencephalographic burst suppression as maximal reduction in
cerebral blood flow and metabolism occurs at this level. The main side
effect remains hypotension and cardiovascular toxicity. Hence when
used it is generally recommended that invasive hemodynamic monitoring
be in place."
The actual data studying barbituate-induced coma is conflicting. A
study by Lee et al (1994), suggests that in patients who fail
conservative therapy, there may be a survival benefit when using a
"The purpose of this study was to evaluate the role of barbiturate
therapy as an adjunctive treatment for control of intracranial
hypertension when conventional methods failed. To this end, a
retrospective chart review was conducted on 21 neurosurgical trauma
patients with uncontrolled intracranial pressure (ICP) admitted to a
trauma/intensive care unit. In this patient population, the overall
mortality was 48%. Control of ICP was achieved in 67% of patients. The
survival of patients experiencing ICP control with barbiturate coma
was better than those patients who failed therapy (71% vs 14%, p =
0.021). Thus, in a subgroup of neurosurgical trauma patients who are
refractory to conventional management of elevated ICP, barbiturates
appear to improve survival, suggesting that this therapy has an
important role in the management of neurotrauma patients." (1)
However, a systematic review by the Cochrane Database finds otherwise:
"Reviewers' conclusions: There is no evidence that barbiturate therapy
in patients with acute severe head injury improves outcome.
Barbiturate therapy results in a fall in blood pressure in 1 in 4
treated patients. The hypotensive effect of barbiturate therapy will
offset any ICP lowering effect on cerebral perfusion pressure."
2) What kinds of setbacks/problems occur if there is swelling of/in
the brain as a result of severe head trauma?
Here are some basic effects from Medline Plus:
Older children and adults:
changes in behavior
progressive decreased consciousness, may become coma
More signs and symptoms can be found on Discovery Health:
"The symptoms of increased intracranial pressure may include: ·
headache · ringing in the ears · nausea and vomiting · vision
problems, such as blurry vision or double vision · feeling tired and
wanting to sleep · painful eye movements · neck pain · hearing loss ·
unsteadiness while standing or walking, known as ataxia · weakness,
which may occur in only certain parts of the body or throughout the
If intracranial pressure is very high, death may occur from brain
injury. Some people have mildly elevated intracranial pressure over a
long time. These people may develop vision or hearing problems."
Herniation of the brain is the most severe effect of increased ICP.
Here is a description of the effects of herniation of different parts
of the brain:
"1. Consequences of Uncal (Temporal Lobe) Herniation
a.Compression of cranial nerve III. The ipsilateral third nerve, as it
passes between the posterior cerebral and superior cerebellar
arteries, is initially flattened and may show hemorrhage. The first
clinical sign is ipsilateral pupil dilation, since the parasympathetic
fibers are located on the outside of the nerve and are inactivated
first by compression. Complete third nerve paralysis may also occur.
As the herniation progresses, the contralateral oculomotor nerve may
be compressed, producing bilateral pupil dilation.
b.Compression of midbrain cerebral peduncles. Most often the
ipsilateral cerebral peduncle is compressed, resulting in
contralateral hemiparesis or hemiplegia. In addition the cerebral
peduncle on the side opposite the space-occupying lesion may be
compressed against, or indented by, the free edge of the tentorium
cerebelli. This results in ipsilateral hemiparesis or hemiplegia (if
it occurs alone) or quadriplegia (if both peduncles are compressed)
c.Compression of the posterior cerebral artery. Obstruction of the
posterior cerebral artery or its branches, due to compression of the
artery against the free edge of the tentorium, produces hemorrhagic
infarction on the medial and inferior aspects of the ipsilateral
occipital lobe (occasionally the infarction is bilateral). Hemorrhagic
infarction occurs because the compression may be reduced after damage
to arterial walls and blood then enters the infarcted area. The lesion
is often confined to the distribution of the calcarine branches of the
posterior cerebral artery. Clinically, cortical blindness is a common
d.Brainstem compression. The patient becomes comatose and may develop
bradycardia secondary to increasing brainstem compression. Decerebrate
posturing in response to noxious stimuli and hyperventilation may be
seen. Secondary brainstem hemorrhages (Duret hemorrhages) may occur,
probably because of compression and stretching of blood vessels,
especially veins. Brainstem decompensation will gradually progress
caudally. As the lower pons and upper medulla are involved, regular,
shallow respirations appear and the extremities become flaccid.
Finally, as the damage in the medulla causes slow irregular
respirations, an irregular pulse and falling blood pressure, death may
occur due to respiratory arrest.
2. Consequences of Central Herniation (Rostrocaudal deterioration)
a. General comments. Rostrocaudal deterioration (or rostrocaudal
decompensation) is the progressive decline in neurological status due
to lesions progressively more caudal as a result of a supratentorial
space occupying mass and downward displacement of the brainstem.
Lesions lying medially or in the frontal pole may not compress the
diencephalon and midbrain laterally, but rather result in rostrocaudal
dysfunction of the brainstem with bilateral progression of impairment.
As in uncal herniation, secondary or Duret hemorrhages may occur in
the midbrain and pons as the brainstem is displaced.
b. Clinical Signs.
i. Changes in consciousness begin with decreasing alertness,
progressing to drowsiness, stupor and coma.
iii. Decorticate rigidity, characterized by leg extension and arm
flexion, results from wide-spread lesions in the cerebral cortex.
Decerebrate rigidity, characterized by extension of both arms and
legs, follows lesions disconnecting the cerebral hemispheres from the
brainstem e.g. lesions in the upper midbrain commonly produce
iv. Pupillary changes in a comatose patient can be used to evaluate
the general location of lesions. Examples of abnormalities include:
Small reactive: Compression of the diencephalon impairs sympathetic
fibers which originate there; impairment of sympathetic mediation of
pupil dilation leads to small pupils. Unilateral Dilated, fixed:
Compression of one oculomotor nerve (III nerve) by the uncus impairs
the parasympathetic fibers travelling along the periphery of the III
nerve; inactivation of these parasympathetic fibers leads to dilation
of the ipsilateral pupil and loss of the light reflex in that pupil.
Bilateral Midposition, fixed: Compression of both III nerves or
compression of the midbrain results in bilateral impairment of both
parasympathetic and sympathetic fibers travelling to the pupil; thus
the pupils are midposition (medium size) and fixed (no light reflex in
3. Consequences of cerebellar tonsil herniation
Displacement of the cerebellar tonsils through the foramen magnum
compresses the medullary respiratory centers, leading to death.
4. Consequences of lateral displacement of brain
Changing levels of consciousness have been correlated with lateral
displacement of diencephalon."
Please use any answer clarification before rating this answer. I will
be happy to explain or expand on any issue you may have.
Internet search strategy using Hotbot.com
barbituate induced coma
induced coma head trauma
effects of intracranial pressure
increased intracranial pressure
barbituate induced coma recommendations
1) Lee, Michael W., et al. "The Efficacy of Barbiturate Coma in the
Management of Uncontrolled Intracranial Hypertension Following
Neurosurgical Trauma." Journal of Neurotrauma 11, no. 3 (1994): 325.
Principal Health News - Barbituate Induced Coma
Trauma.org - Barbituate Coma
Trauma.org - Intracranial Pressure
Medline Plus - Increased Intracranial Pressure
Discovery Health - Increased Intracranial Pressure