Neurological Case Study 3

 

A 23-year-old male student from Thailand studying electrical engineering at the university was ejected from a moving vehicle, which was traveling 70 mph. His injuries included a severe closed head injury with an occipital hematoma, bilateral wrist fractures, and a Right pneumothorax. During his NICU stay, this client was intubated and placed on mechanical ventilation, had a feeding tube inserted and was placed on tube feedings, had a Foley catheter to dependent drainage, and had multiple IVs inserted. He developed pneumonia 1 month after admission.

 

  1. Describe the term Primary head injury.

 

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.

 

 

  1. Describe secondary head injury.

 

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

 

 

  1. Why is increased intracranial pressure (IICP) so clinically important? What are five signs and symptoms of IICP?

 

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

B.    Bradycardia

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).

 

 

  1. List four medication classifications and eight nursing measures that the ICU nurses could use to control or decrease the ICP.

 

Eight Nursing Interventions that can be used to help control/decrease ICP include:

 

    • Perform neurological assessments hourly.
    • Elevate the HOB 15-30 degrees.
    • Monitor neurological responses to any activities that increase ICP.
    • Maintain the head in a neutral (midline) position.
    • Avoid extreme hip flexion, isometric exercise, straining with stool, breath-holding exercices.
    • Observe strict fluid restrictions (as ordered by MD, ARNP, or PA).
    • Do NOT suction for more than 15 seconds at a time; utilize hyperoxygenation before and after procedure.
    • Perfom Neurological Assessments qh.

 

Four medication classes used to help control/decrease ICP include:

 

  • Diuretics:  Osmotic Diuretics (Mannitol®) helps to draw water from the brain cells and into the plasma. Loop Diuretics (Lasix®, Bumex®) decrease ICP by removing Na+ and water from injured brain cells and decreasing CSF formation. Watch for electrolyte imbalance with the use of these drugs.

 

  • Corticosteroids: Decadron® is the most commonly used corticosteroid used to reduce cerebral edema; however, research on its effects on decreasing ICP alone yields mixed results. Watch for electrolyte disturbances along with hyperglycemia and immunosuppression.

 

  • Anticonvulsants: Because of the increased risk for seizure activity of brain injury patients, antiepileptic agents such as Dilantin® and Tegretol® are used to help increase the threshold of excitation among neurons, which decreases seizure risk. Watch for ataxia and lethargy along with gingival hyperplasia with prolonged Dilantin® use. Dilantin® is given IV through a filtration device and the patient must be monitored closely for heart block.

 

  • Antihypertensives: Hypotension causes a decrease in cerebral blood flow, which leads to cerebral ischemia.  HTN > 160 mm Hg can lead to cerebral ischemia as a result of cerebral vessel compression. Antihypertensives such as Beta-Blockers, Ca-Channel Blockers, and ACE-Inhibitors can decrease overall BP. Watch for bradycardia and hypotenstion as an adverse effect.

 

 

  1. This client’s medications include clindamycin (Cleocin) 150 mg per feeding tube q6h, ranitidine (Zantac elixir) 150 mg per feeding tube BID, and phenytoin (Dilantin) 100 IVPB tid. Indicate why he is on each medication.

 

This client is taking the following medications for the following indications:

 

    • Cleocin®: This is a Miscellaneous Anti-Infective agent used to treat respiratory tract infections with bacterial etiology.  This agent will help to inhibit protein synthesis at the level of the 50S Ribosomem resulting in bactericidal or bacteriostatic action. It is being used for this patient’s pneumonia. Adverse effects include Diarrhea, C. diff colitis, dizziness, and dysrhythmias.

 

    • Zantac®: This is an H2 Blocking agent used to decrease acid secretion in the stomach. ICU patients are prone to develop a painless, slow-bleeding ulcer known as a Curling’s Ulcer or Stress Ulcer. This agent helps to reduce this risk. HA is the most common adverse effect.

 

    • Dilantin®: This is an antiepileptic medication used to control seizure activity. Any change in the physiologic integrity of the brain can decrease the threshold of excitation and result in hyper-firing of neurons, leading to seizure. Dilantin® is used to increase this threshold and decrease seizure activity. Common adverse effects include ataxia, drowsiness, gingival hyperplasia, and heart block (on IV infusion therapy).

 

 


  1. A STAT portable chest x-ray (CXR) is ordered after each central venous catheter (CVC) is inserted. According to hospital protocol, no one is permitted to infuse anything through the catheter until the CXR has been read by the physician or radiologist. What is the purpose of the CXR and why isn’t fluid infused through the catheter until after the CXR is read?

 

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 Thailand.

 

  1. His latest lab results are as follows:
    • Na 149 mmol/L                                 (135-145 mmol/L)
    • K 4.2 mmol/L                                    (3.5-5.5 mmol/L)
    • Cl 119 mmol/L                                  (97-107 mEq/L)
    • BUN 12 mg/dl                                   (5-18 mg/dl)
    • Creatinine 1.2 mg/dl                         (.8-1.5 mg/dl)
    • Glucose 123 mg/dl                           (80-120 mg/dl)
    • WBC 15.4 thousand/cmm                (5,000-10,000/cmm)
    • Hgb 14.9 g/dl                                    (12-15 g/dl)
    • Hct 36.4%                                         (37%-47%F; 40%-54%M)
    • Platelets 140 thou/cmm                    (150,000-400,000 mm3)

Are any of these a concern to you, and what would you suggest to correct     them? 

    • Na+ 149 mmol/L: This is Hypernatremia—watch for cardiac dysrhythmias and s/s of dehydration, which can cause cerebral cell crenation.

 

    • Cl 119 mmol/L: This is an elevated chloride level. This is correlated with the Hypernatremia seen above. Again, watch for dysrhythmias, impaired mentation, HTN/Hypotension.

 

    • WBC 15.4 thousand/cmm: This is leukocytosis—associated with the client’s pneumonia, which is in the process of resolving.

 

 


  1. Are you surprised by his agitated behavior? Explain.

 

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.

 

 

 

  1. Outline a general rehabilitation plan for this client based on the above data.

 

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.

 

 

  1. This client’s mother has just arrived in the United States and speaks no English. What measures can be taken to facilitate communication between medical personnel and the mother?

 

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.

 

 

 

  1. What special discharge planning considers are there in this case?

 

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.