3.

Cause of the woman loss of consciousness and relation about a torn wound in the right
temple?
Scalp Wounds

The scalp is highly vascular and often bleeds briskly when lacerated. Because many of the small
blood vessels arc suspended in an inelastic matrix of supporting tissue, the normal protective
vasospasm that would limit bleeding is inhibited, which may lead to prolonged bleeding and
significant blood loss. This can be very important in children who bleed as freely as adults but do
not have the same blood volume. Though an un common cause of shock in adult. a child may
develop shock from a briskly bleeding scalp wound. As a general rule, if you have an adult palient
with a scalp injury who is in shock, look for an other cause for the shock (such as internal bleeding).
However, do not underestimate the blood loss from a scalp wound. Most bleeding from the scalp
can be easily, controlled in the field with direct pressure if your exam reveals no unstable fractures
under the wound.

Intracranial Hemorrhage: Hemorrhage can occur between the skull and dura (the fibrous covering
of the brain ), between the dura and the arachnoid, or directly into the brain tissue.

Acute Epidural Hematoma: An acute epidural hematoma is most often caused by a tear in the
middle meningeal artery that runs along the inside of the skull in the temporal region. The arterial
injury is often caused by a linear skull fracture in the temporal or parietal region. Because the
bleeding is arterial (although it may be venous from one of the dural sinuses), the bleeding and
rise in ICP can occur rapidly, and death may occur quickly.

Symptoms of an acute epidural hematoma include a history of head trauma with initial loss of
consciousness often followed by a period during which the patient is conscious and coherent (the
"lucid interval"). After a period of a few minu tes to several hours, the patient will develop signs
of increasing ICP (vomiting, headache, altered mental status), lapse into unconsciousness, and
develop body paralys is on the side opposite of the head. There is often a dilated and fixed (no
response to bright light) pupil on the side of the head injury. These signs are usually followed
rapidly by death.

Acute Subdural Hematoma: This is the result of bleeding between the dura and the arachnoid and
is associated with injury to the underlying brain tissue. Because the bleeding is venous, intracranial
pressure increase more slowly, and the diagnosis often is not apparent until hours or days after the
injury. The signs and symptoms include headache, fluctuations in the level of consciousness, and
focal neurologic signs (e.g., weakness of one extremity or one side of the body, altered deep tendon
reflexes, and slurred speech). Because of underlying brain tissue injury, prognosis is often poor.
Mortality is vcry high (60 percent- 90 percent) in patients who are comatose when found. Always
suspect a subdural hematoma in an alcoholic with any degree of altered mental status following a
fall. Elderly patients and those taking anticoagulants are also at high risk for this injury.
Intracerebal Hemorrhage: Intracerebral hemorrhage is bleeding with in the brain tissue. Traumatic
intracerebral hemorrhage may result from blunt or penetrating injuries of the head. Unfortunately,
surgery is often not helpful. The signs and symptoms depend upon the regions involved and the
degree of injury. They occur in patterns similar to those that accompany a stroke; spontaneous
hemorrhages of this type may be seen in patients with severe hypertension. Alteration in the level
of consciousness is commonly seen, though awake patients may complain of headache and
vomiting.

Refrences : John Emory Campbell. 2008. International Trauma Life Support for Prehospital Care
Provider
11. Farmacology treatment

Osmotic Agents

Additional therapy for increased ICP includes the use of osmotic diuretics, such as mannitol and
HTS (Hypertonic Saline). With deepening coma, pupil inequality, or other deterioration of the
neurologic examination, osmotic agents may be lifesaving. Mannitol is the mainstay for control of
elevated ICP in acute severe TBI (Traumatic Brain Injury). The Brain Trauma Foundation and the
European Brain Injury Consortium recommend mannitol as the osmotic drug of choice. However,
few comparative data exist on mannitol and other ICP-lowering medications. A Cochrane database
review concluded that mannitol may have a small beneficial effect compared with pentobarbital.59
ICP-directed therapy based on neurologic signs may also be beneficial. However, other evidence
suggests that mannitol may be detrimental compared with HTS. Further research is needed on
optimal osmotic therapy in severe head trauma.

Mannitol (0.25-1 g/kg) can effectively reduce cerebral edema by producing an osmotic gradient
that prevents the movement of water from the vascular space into the cells during membrane pump
failure and draws tissue water into the vascular space. This reduces brain volume and provides
increased space for an expanding hematoma or brain swelling. The osmotic effects of mannitol
occur within minutes and peak approximately 60 minutes after bolus administration. The ICP-
lowering effects of a single bolus may last for 6 to 8 hours. Mannitol has many other
neuroprotective properties. It is an effective volume expander in the presence of hypovolemic
hypotension and therefore may maintain systemic blood pressure required for adequate cerebral
perfusion. It also promotes CBF by reducing blood viscosity and microcirculatory resistance. It is
an effective free radical scavenger, reducing the concentration of oxygen free radicals that may
promote cell membrane lipid peroxidation. However, mannitol can produce renal failure or
hypotension if given in large doses. It may also induce a paradoxical effect of increased bleeding
into a traumatic lesion by decompressing the tamponade effect of a hematoma. Because of these
and other potential problems, the use of mannitol should be reserved for head-injured patients with
evidence of increasing ICP and neurologic deterioration
Barbiturates

Barbiturate therapy is occasionally used in severely head-injured patients to reduce cerebral

metabolic demands of the injured brain tissue. Barbiturates also affect vascular tone and inhibit
free radicalmediated cell membrane lipid peroxidation. The effects of barbiturates are delayed
relative to other acute interventions for reducing ICP; therefore they are rarely initiated in the ED.
If other methods of reducing ICP have been unsuccessful, barbiturates may be added in the
hemodynamically stable patient. Pentobarbital is the barbiturate most often used

Seizure Prophylaxis

Up to 12% of all patients who sustain blunt head trauma and 50% of those with penetrating head
injury develop early post-traumatic seizures (PTSs). Although the occurrence of seizures in the
immediate post-trauma period has no predictive value for future epilepsy, early seizures can cause
hypoxia, hypercarbia, release of excitatory neurotransmitters, and increased ICP, which can
worsen secondary brain injury. Constantly firing neurons are soon depleted of their energy sources,
and in the head trauma patient with compromised cerebral metabolism, uncontrolled seizures
exacerbate the neurologic deficit. If the patient is actively seizing, benzodiazepines are
administered as effective, rapid-acting first-line anticonvulsants. Lorazepam (0.05-0.1 mg/kg IV
over 2-5 minutes up to a total of 4 mg) has been found to be most effective at aborting status
epilepticus. Diazepam (0.1 mg/kg, up to 5 mg IV, every 10 minutes up to a total of 20 mg) is an
alternative. For long-term anticonvulsant activity, phenytoin (18-20 mg/kg IV) or fosphenytoin
(15-18 phenytoin equivalents/kg) can be given.
Refrences : Marx, John A. 2014. Rosens Emergency Medicine. Vol 1. 8th Ed