TBI in Adult and Pet Case - Nursing Assignments/ Essays/Case Study for Nursing Students

Hi all,

I am a registered nurse based in Melbourne and I have been helping Nursing Students with their coursework since 10 years.

I can help with the following:

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I am putting here one of my work. This will give you an idea about how to frame the answer and what details should be used?

Introduction

The consequences of fall and associated traumatic brain injury can be lethal to both children

and adults. This is because, one of the most common complication is increased intracranial

pressure which in turn is a life-taking sign and escalation points to clinical deterioration. This

essay discusses case of Leo (adult) and Tamara (paediatric) client with TBI and SAH. The

first part explains the pathophysiology and associated clinical cues whereas the second part

discusses the role of family in recognising and responding to acute deterioration (NSQHS

standard 9).

Vital signs and pathophysiology of increased ICP

Traumatic brain injury and physiological dysfunction results in growing pressure inside the

skull. This is termed as increased intracranial pressure and is a life-threatening situation. An

Intracranial pressure greater than 20mmg is labelled as increased ICP and that is dangerous to

survival (Pinto et al., 2018). The ICP>20mmHg causes downward herniation of the uncus

through the tentorial notch. This results in compression in the three main areas of brain;

compression of midbrain, pons and medulla. The compression of the midbrain in turn is

responsible for the compression of reticular formation and periaqueductal grey (Macdonald &

Schweizer, 2017, pp. 656). This is responsible for the reduced level of consciousness and

Glasgow coma scale, evident as responsive to speech, confusion words and GCS score of 12

(Svedung et al., 2020, pp. e0197).

The compression of pons consequently results in compression of cranial nerve 6 as

cranial nerve VI is vulnerable to be compressed due to its long course and acute bend through

the Dorello’s canal. The compression of 6 th CN causes diplopia on the horizontal gaze. There

is also compression of medulla; with subsequent herniation through the foramen magnum

would be a late occurrence (Emelifeonwu et al., 2018, pp. 677). In addition, in SAH induced

increased ICP, the right eye non-reactivity and droopiness is due to 3 rd CN palsy seen in

Leo’s case (Emelifeonwu et al., 2018, pp. 677). The compression of medulla stimulates area

postrema and chemoreceptor trigger zone which results in constant feeling of nausea and

vomiting (Talukder et al., 2021).

With increased ICP there is also accumulation of blood, tissue, cerebrospinal fluid or

pus causing compression of optic nerve, the arterioles and the pain receptors in vessels and

meninges. In optic nerve, there is obstruction of axoplasmic flow withing optic nerve. This

leads to severe axonal swelling and causes leakage of cellular contents into the optic disc

space (Bingöl & Atilla, 2021, pp. 418). This produces two major signs; spells of reduced

visual acuity and papilledema (Bingöl & Atilla, 2021, pp. 418).