Chapter 23 Flashcards
Description and etiology
Patho
Assessment and dx
Medical management
Nursing management
Coma
Normal consciousness requires awareness and arousal.
Awareness is the combination of cognition (mental and intellectual) and affect (mood) that can be construed based on the patient’s interaction with the environment. Alterations of consciousness may be the result of deficits in awareness, arousal, or both.
Coma is characterized by the absence of both wakefulness and awareness, Coma is the deepest state of unconsciousness; arousal and awareness are lacking. The patient cannot be aroused and does not demonstrate any purposeful response to the surrounding environment. Coma is a symptom rather than a disease, and it occurs as a result of some underlying process.
causes of coma can be divided into two general categories: structural or surgical and metabolic or medical.
Structural causes of coma include ischemic stroke, ICH, trauma, and brain tumors. Metabolic causes of coma include drug overdose, infectious diseases, endocrine disorders, and poisonings. The three most common causes of nontraumatic coma are stroke, anoxia, and poisonings. Coma demands immediate attention, resulting in a high percentage of admissions to all hospital services.
Description and etiology - Coma
Consciousness involves arousal, or wakefulness, and awareness.
Neither of these functions is present in a patient in coma.
Structural causes usually produce compression or dysfunction in the area of the ascending reticular activating system (RAS), whereas most medical causes lead to general dysfunction of both cerebral hemispheres. Trauma, hemorrhage, and tumor can damage the ascending RAS, leading to coma. Destruction of large regions of bilateral cerebral hemispheres can be the result of seizures or viral agents. Toxic drugs, toxins, or metabolic abnormalities can suppress cerebral function.
Patho - Coma
Structural causes usually produce compression or dysfunction in the area of the ascending RAS, whereas most medical causes lead to general dysfunction of both cerebral hemispheres. Trauma, hemorrhage, and tumor can damage the ascending RAS, leading to coma. Destruction of large regions of bilateral cerebral hemispheres can be the result of seizures or viral agents. Toxic drugs, toxins, or metabolic abnormalities can suppress cerebral function.
Medical history is essential,Detailed serial neurologic examinations are essential for all patients in coma.
Assessment of pupillary size and reaction to light (normal, sluggish, or fixed), extraocular eye movements (normal, asymmetric, or absent), motor response to pain (normal, decorticate, decerebrate, or flaccid), and breathing pattern yields important clues for determining whether the cause of coma is structural or metabolic.
Deficits in extraocular eye movements usually accompany a structural cause.
Focal or asymmetric motor deficits usually indicate structural lesions.
Abnormal breathing patterns may also assist in differentiating structural from metabolic causes of coma. Cheyne Stokes respirations are seen in patients with cerebral hemispheric dysfunction or metabolic suppression. Central neurogenic hyperventilation, or Kussmaul breathing, occurs with metabolic acidosis or damage to the midbrain and upper pons. Apneustic breathing may occur with damage to the pons, hypoglycemia, and anoxia. Ataxic breathing occurs with damage to the medulla. Agonal breathing occurs with failure of the respiratory centers in the medulla.
laboratory studies and diagnostic procedures are done.
Structural causes of coma are usually readily apparent with CT or MRI. Laboratory studies are also used to identify metabolic or endocrine abnormalities.
An electroencephalogram should be obtained to search for sleep patterns, particularly rapid eye movement sleep and slow-wave sleep. A positron emission tomography scan may also be helpful in detecting consciousness.
Assessment and dx - Coma
is identification and treatment of the underlying cause of the condition.
Initial medical management includes emergency measures to support vital functions and prevent further neurologic deterioration. Protection of the airway and ventilatory assistance are often needed. Administration of thiamine
Intubation for continued airway protection and nutrition support is essential. Fluid and electrolyte management is often complex because of alterations in the neurohormonal system. Anticonvulsant therapy may be necessary to prevent further ischemic damage to the brain.
Prognosis depends on the cause of coma and the length of time unconsciousness persists.
Medical management - Coma
A patient care management plan for a patient in coma incorporates a variety of patient problems and is directed by the specific cause of coma, although some common interventions are used.
a significant role in monitoring for changes in neurologic status and clues to the origin of coma, supporting all body functions, maintaining surveillance for complications, providing comfort and emotional support, and initiating rehabilitation measures. Measures to support body functions include promoting pulmonary hygiene, maintaining skin integrity, initiating range-of-motion exercises, managing bowel and bladder functions, and ensuring adequate nutrition support.
Nursing management - Coma
A craniotomy is performed to gain access to portions of the central nervous system (CNS) inside the cranium, usually to allow removal of a space-occupying lesion
Common procedures include tumor resection or removal, cerebral decompression, evacuation of hematoma or abscess, and clipping or removal of an aneurysm or AVM.
Patients who do require such care usually need intensive monitoring or are at greater risk for complications because of underlying cardiopulmonary dysfunction or the surgical approach used.
provides definitions of common neurosurgical terms.
Types of surgery - Craniotomy
Protection of the integrity of the CNS is a major priority of care for a patient awaiting a craniotomy. Optimal arterial oxygenation, hemodynamic stability, and cerebral perfusion are essential for maintaining adequate cerebral oxygenation. Management of seizure activity is essential for controlling metabolic needs. Detailed assessment and documentation of the patient’s preoperative neurologic status are imperative for accurate postoperative evaluation.
Preoperative teaching is necessary to prepare the patient and family for what to expect in the postoperative period. A description of the intravascular lines and intracranial catheters used during the postoperative period allows the family to focus on the patient and not be overwhelmed by masses of tubing.
All patients who undergo craniotomy require instruction to avoid activities known to provoke sudden changes in ICP.
These activities include bending, lifting, straining, and the Valsalva maneuver.
Patients undergoing transsphenoidal surgery require preparation for the sensations associated with nasal packing. Preoperative instruction in mouth breathing and avoidance of coughing, sneezing, or blowing of the nose facilitates postoperative cooperation.
Preop care - Craniotomy
Depending on the location of the lesion and the surgical route chosen, a transcranial or a transsphenoidal approach is used to open the skull.
Surgical considerations - Craniotomy
Definitive management of a postoperative neurosurgical patient varies depending on the underlying reason for the craniotomy.
During the initial postoperative period, management is usually directed toward the prevention of complications. Complications associated with a craniotomy include intracranial hypertension, surgical hemorrhage, fluid imbalance, CSF leak, and DVT.
Intracranial HTN
Cerebrospinal fluid leak
DVT
Postop nursing management
Postop medical management - Craniotomy
Postoperative cerebral edema is expected to peak 48 to 72 hours after surgery.
Close monitoring of the surgical site is important so that integrity of the incision can be maintained. Management of intracranial hypertension after craniotomy is usually accomplished through CSF drainage, patient positioning, and steroid administration.
Intracranial HTN
after a transcranial procedure can occur in the intracranial vault and manifests as signs and symptoms of increasing ICP. Hemorrhage after a transsphenoidal craniotomy may be evident from external drainage, the patient’s complaint of persistent postnasal drip, or excessive swallowing. Loss of vision after pituitary surgery indicates an evolving hemorrhage. Postoperative hemorrhage requires surgical reexploration
Surgical hemorrhage
usually results from a disturbance in production or secretion of antidiuretic hormone (ADH).
The outcome is unabated renal water loss even when blood volume is low and serum osmolality is high. This condition is known as diabetes insipidus (DI). The polyuria associated with DI is often more than 200 mL/h. Urine specific gravity of 1.005 or less and elevated serum osmolality provide evidence of insufficient ADH. The loss of volume may provoke hypotension and inadequate cerebral perfusion. DI is usually self-limiting, and fluid replacement is the only required therapy. However, in some cases, it may be necessary to administer vasopressin intravenously to
control the loss of fluid.
SIADH manifests as inappropriate water retention with hyponatremia in the presence of normal renal function. Urine specific gravity is elevated, and urine osmolality is greater than serum osmolality. The dangers associated with SIADH include circulating volume overload and electrolyte imbalance, both of which may impair neurologic functioning. SIADH is usually self-limiting, with the mainstay of treatment being fluid restriction.
Fluid imbalance
Leakage of CSF results from an opening in the subarachnoid space, as evidenced by clear fluid draining from the surgical site. When this complication occurs after transsphenoidal surgery, it is evidenced by excessive, clear drainage from the nose or persistent postnasal drip. To differentiate CSF drainage from post-operative serous drainage, a specimen is tested for glucose content.
Management of a patient with a CSF leak includes bed rest and head elevation.
Cerebrospinal fluid leak
have a variety of additional risk factors, including preoperative leg weakness, longer preoperative and postoperative stay in the critical care unit, longer operative procedure time, prone positioning on frames with flexion of the hips or knees, longer time in the postanesthesia care unit, more days on bed rest, lengthy operative procedures, and delay of postoperative mobility and activity.
DVT
The nurse has a significant role in preserving adequate CPP, promoting arterial oxygenation, providing comfort and emotional support, maintaining surveillance for complications, initiating early rehabilitation, and educating the patient and family.
Frequent neurologic assessment is necessary to evaluate accomplishment of these objectives and to identify problems and quickly intervene if complications do arise. A ventriculostomy often is placed to facilitate ICP monitoring and CSF drainage.
Preserve cerebral perfusion
Promote arterial oxygenation
Provide comfort and emotional support
Initiate early rehabilitation
Educate the patient and family
Postop nursing management
patient positioning, fluid management, and avoidance of post-operative vomiting and fever.
Positioning
Fluid management
Avoidance of vomiting and fever
Preserve cerebral perfusion
head of the bed should always be elevated to 30 to 45 degrees to reduce the incidence of hemorrhage, facilitate venous drainage, and control ICP.
These rules of positioning must be followed through-out all nursing activities, including linen changes and transporting the patient for diagnostic evaluation.
Positioning
is another important component of postcraniotomy care. Hourly monitoring of fluid intake and output facilitates early identification of fluid imbalance. Urine specific gravity must be measured if DI is suspected. Fluid restriction may be ordered as a routine measure to lessen the severity of cerebral edema or as treatment for the fluid and electrolyte imbalances associated with SIADH.
Fluid management
