Neurological Case Study 3
A 23-year-old male student
A Primary Head Injury is the result of deformation of the brain at the point of impact by a small object such as a hammer, a rock or a golf ball. The result is injury to the scalp and a skull fracture. This could be associated with dural laceration and underlying brain contusion or laceration. Usually there is a localized surrounding edema around the site of the impact.
A Secondary Head Injury results as a sequelae to the primary brain injury and includes:
A Intracranial Hematomas:
The intracranial hematomas are divided into:
1 EPIDURAL HEMATOMA:
Caused by a tear in the middle meningeal artery with blood clot collected between the dura and the overlying bone. In about 60 or 70% of cases there is an associated skull fracture. Usually the clot is located in the temporal area. Occasionally it is in the frontal, parietal or posterior fossa region. As it is an arterial bleed, the clot can get to a significant size within a short period of time with rapid rise in the intracranial pressure. If untreated there is a high rate of morbidity and mortality but effective and early treatment can result in complete recovery. In these cases there is no diffuse brain injury and the injury is localized to the area where the fracture and the hematoma is located. The aim of the management is to evacuate the clot as soon as possible and control the bleeding meningeal vessel.
In most cases this is an acute condition, however occasionally the bleeding is a result of venous tear and the blood clot develops slowly. This is particularly the case in the frontal and occipital regions. The clot is evacuated through a craniotomy but in acute situations where there are no facilities for major neurosurgical procedure a burr hole should be done to release the intracranial clot and reduce the intracranial pressure.
2. SUBDURAL HEMATOMA:
This is the result of tear in one of the bridging veins between the surface of the cortex and the dural sinuses. The blood collects gradually and slowly as the bleed is of venous origin. Acute subdural haematomas are rare in children. These haematomas are usually a part of severe and diffuse brain injury. It results with significant morbidity and mortality because of associated diffuse brain injury.
3. Brain Edema; 4. Infection 5. Hydrocephalus; 6. Leakage of CSF
Intracranial Pressure is a very important clinical indicator of patient presentation, severity of condition, and overall prognosis. In addition, measurements of ICP can help indicate positive or negative responses to interventions. Raised ICP can cause Cushing’s Triad:
A. Arterial hypertension
C. Respiratory changes
It is traditionally accepted that hypertension and bradycardia are due to ischemia or pressure on the brainstem. There is also a suggestion that they could be due to removal of supratentorial inhibition of brainstem vasopressor centers due to cerebral ischemia and that bradycardia is independent of the rise in blood pressure.
The respiratory changes depend on the level of brainstem involvement. The midbrain involvement result in Chyne-Stokes respiration. When midbrain and pons are involved, there is sustained hyperventilation. There is rapid and shallow respiration when upper medulla involvement with ataxic breathing in the final stages.
Pulmonary edema seems to be due to increased sympathetic activity as a result of the effects of raised ICP on the hypothalamus, medulla or cervical spinal cord. In addition to these four symptoms, N/V (Projectile in nature) and HA are also classic signs of increased ICP. ICP > 16 mmHg is considered increased (Sole, et, al, 2001).
Eight Nursing Interventions that can be used to help control/decrease ICP include:
Four medication classes used to help control/decrease ICP include:
This client is taking the following medications for the following indications:
This CXR is designed to ensure proper placement of the catheter tip and also to ensure the absence of pneumothorax. No medications, fluids, etc. is given through the line before obtaining the approval of the Radiologist, MD, ARNP, or PA.
This client has spent 2
months in acute care and is now on your rehab unit. He follows commands but
tends to get very agitated with too much stimulation. His trach site is well
healed and the pneumonia is finally resolving. He is still receiving
supplemental tube feeding and has some continued incontinence of the both bowel
and bladder. He has a very supportive group of friends at the university;
several of them are also from
Are any of these a concern to you, and what would you suggest to correct them?
This patient’s agitation is probably resulting from activities that cause hypoxemia or increased ICP. The environment should be kept as stimuli-free as possible and the patient should have the HOB elevated 15-30 degrees with adequate oxygenation.
Depending on the course of recovery, this patient may need to be placed in a long-term care facility. Occupational Therapists should be consulted to assist the patient’s functional capacity in meeting ADLs and Physical Therapists should be consulted to assess and assist with mobility and ROM concerns. In the acute interim, the patient needs adequate periods of rest, adequate oxygenation, and ADL provisions.
Proper communication for this patient is facilitated with a certified translator of the mother’s native language. Other forms of translators (hospital employees, etc.) are sometimes used in different capacities; buyt NCLEX requires a certified interpreter.
Long-term care needs of this client need to be assessed. In addition, this client may need care providers and it will be salient to assess the abilities of each one of these providers in assisting him with ADLs, meeting medical demands and requirements, etc. He will need long-term collaborative therapy with speech pathologists, occupational and physical therapists, and other members of the medical team.