Southern Luzon State University College of Allied Medicine Lucban, Quezon
Bilateral Subdural Hematoma with Subacute Component s/p Bilateral Silver Dollar Craniectomy (Surgical Decompression) (Case Study)
In Partial Fulfillment of the Requirements in the NCM 105 Related Learning Experience
Presented by: Roeder Max R. Pangramuyen BSN III Group 9
Presented to: Prof. Rosalinda A. Abuy RN, MAN Clinical Instructor
May 3, 2013
I.
OBJECTIVES A. GENERAL OBJECTIVE
After
establishing establish ing a
nurse-patient nurse-pati ent
interaction, interactio n,
providing providin g
different nursing
interventions and care to the client and by thorough assessment and careful study about the patient’s condition, student will gain knowledge, develop skills and enhance
attitude through the utilization of the nursing process on the care and management for the patient with subdural hematoma with sub-acute component.
B.
SPECIFIC OBJECTIVES
1. Define what Subdural Hematoma is. 2. Discuss the causes and risk factors for Subdural Hematoma. 3. Study the diagnostic procedures and medical and surgical treatment of the disease. 4. Trace the pathophysiology of the disease. 5. Determine the health status of the patient through: i. General Data ii. Physical Assessment iii. Present History of Illness iv. Family Health History v. Personal and Social History 6. Establish a good nurse-patient relationship. 7. Analyze laboratory results and correlate it with the patient’s present condition. 8. Familiarize self to some medical and diagnostic procedures related to the patient’s present condition.
9. Determine the relevance of the drugs or medications to the patient’s condition. 10. Formulate nursing diagnoses and provide the necessary nursing management and intervention based on the clinical manifestations presented by the patient’s
needs and problems. 11. Evaluate the effectiveness of the nursing care plan and medical management.
II.
INTRODUCTION
The nervous system, the body’s most complex system, profoundly affects both
psychological and physiologic functions. Even more fascinating is the knowledge of man’s ability to comprehend, learn, act and feel as individual organism.
The onset of neurologic disorders may be sudden or insidious. These disorders can be frightening, even devastating, the clients and their significant others- especially if the process is irreversible.
Providing nursing care for the clients with neurologic disorders is challenging and demands extensive knowledge.
One of these distressing disorders is subdural hematoma. A subdural hematoma (SDH) is a collection of blood below the inner layer of the dura but external to the brain and arachnoid membrane. Subdural hematoma is the most common type of traumatic intracranial mass lesion.
Subdural hematoma occurs not only in patients with severe head injury but also in patients with less severe head injuries, particularly those who are elderly or who are receiving anticoagulants. Subdural hematoma may also be spontaneous or caused by a procedure, such as a lumbar puncture Rates of mortality and morbidity can be high, even with the best medical and neurosurgical care.
Subdural hematomas are usually characterized on the basis of their size and location and the amount of time elapsed since the inciting event age (ie, whether they are acute, subacute, or chronic). When the inciting event is unknown, the appearance of the hematoma on neuroimaging studies can help determine when the hematoma occurred. These factors, as well as the neurologic and medical condition of the patient, determine the course of treatment and may also influence the outcome.
Generally, acute subdural hematomas are less than 72 hours old and are hyperdense compared with the brain on computed tomography scans. The subacute phase begins 3-7 days after acute injury. Chronic subdural hematomas develop over the course of weeks and are hypodense compared with the brain. However, subdural hematomas may be mixed in nature, such as when acute bleeding has occurred into a chronic subdural hematoma.
Presentation varies widely in acute subdural hematoma. Many of these patients are comatose on admission. However, approximately 50% of patients with head injuries who require emergency neurosurgery present with head injuries that are classified as moderate or mild (Glasgow Coma Scale scores 9-13 and 14-15, respectively). Many of these patients harbor intracranial mass lesions.
In a large series of patients who developed intracranial hematomas requiring emergent decompression, more than half had lucid intervals and were able to make conversation between the time of their injury and subsequent deterioration. In a more comprehensive review of the literature on the surgical treatment of acute subdural hematomas, lucid intervals were noted in up to 38% of cases.
Acute subdural hematoma is commonly associated with extensive primary brain injury. In one study, 82% of comatose patients with acute subdural hematomas had parenchymal contusions.The severity of the diffuse parenchymal injury shows a strong inverse correlation with the outcome of the patient.In recognition of this fact, a subdural hematoma that is not associated with an underlying brain injury is sometimes termed a simple or pure subdural hematoma. The term complicated has been applied to subdural hematomas in which a significant injury of the underlying brain has also been identified. Acute subdural hematoma is the most common type of traumatic intracranial hematoma, occurring in 24% of patients who present comatose. This type of head injury also is strongly associated with delayed brain damage, later demonstrated on CT scan. Such presentations portend devastating outcomes, and overall mortality rates are usually quoted at around 60%.
Significant trauma is not the only cause of subdural hematoma. Chronic subdural hematoma can occur in the elderly after apparently insignificant head trauma. Often, the antecedent event is never recognized. Chronic subdural hematoma is a common treatable cause of dementia. A minority of chronic subdural hematoma cases derived from acute subdural hematomas that have matured (ie, liquefied) because of lack of treatment.
The head trauma may also cause associated brain hematomas or contusions, subarachnoid hemorrhage, and diffuse axonal injury. Secondary brain injuries may include edema, infarction, secondary hemorrhage, and brain herniation.
Typically, low-pressure venous bleeding from bridging veins dissects the arachnoid away from the dura, and the blood layers out along the cerebral convexity.
Cerebral injury results from direct pressure, increased intracranial pressure (ICP), or associated intraparenchymal insults.
In the subacute phase, the clotted blood liquefies. Occasionally, the cellular elements layer can appear on CT imaging as a hematocrit-like effect. In the chronic phase, cellular elements have disintegrated, and a collection of serous fluid remains in the subdural space. In rare cases, calcification develops.
Much less common causes of subdural hematoma involve coagulopathies and ruptured intracranial aneurysms. Subdural hematomas have even been reported to be caused by intracranial tumors.
It has been asserted that the primary brain injury associated with subdural hematoma plays a major role in mortality. However, most subdural hematomas are thought to result from torn bridging veins, as judged by surgery or autopsy. Furthermore, not all subdural hematomas are associated with diffuse parenchymal injury. As mentioned earlier, many patients who sustain these lesions are able to speak before their condition deteriorates —an unlikely scenario in patients who sustain diffuse damage.
Using a primate model, Gennarelli and Thibault demonstrated that the rate of acceleration-deceleration of the head was the major determinant of bridging vein failure. By using an apparatus that controlled head movement and minimized impact or contact phenomena, they were able to produce acute subdural hematomas in rhesus monkeys. In all cases, the sagittal movement of the head produced by an angular acceleration caused rupture of parasagittal bridging veins and an overlying subdural hematoma.
Gennarelli and Thibault reported that their results were consistent with the clinical causes of subdural hematoma, in that 72% are associated with falls and assaults and only 24% are associated with vehicular trauma. The acceleration (or deceleration) rates caused by falls and assaults are greater than those caused by the energy-absorbing mechanisms in cars, such as dashboard padding, deformable steering wheels, and laminated windshields.
III.
OVERVIEW OF THE DISEASE
Definition
A subdural hematoma also known as subdural hemorrhage (SDH) is a collection of blood accumulating in the potential space between the dura and arachnoid mater of the meninges around the brain. In a subdural hematoma, blood collects between the layers of tissue that surround the brain. The outermost layer is called the dura. In a subdural hematoma, bleeding occurs between the dura and the next layer, the arachnoid. The bleeding in a subdural hematoma is under the skull and outside the brain, not in the brain itself however, when blood accumulates, pressure on the brain increases. The pressure on the brain causes a subdural hematoma's symptoms. If pressure inside the skull rises to very high level, a subdural hematoma can lead to unconsciousness and death. Classification
Subdural hematomas are divided into (a) acute, (b) subacute, and (c) chronic, depending on the speed of their onset. Acute subdural hematomas that are due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression.
Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. They are most severe if associated with cerebral contusions. Acute subdural bleeds have a high mortality rate, higher even than
epidural
hematomas
and diffuse
brain
injuries,
because
the
force
(acceleration/deceleration) required causing those causes other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80%. Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". Chronic subdural hematomas are common in the elderly.
Mortality/Morbidity
Acute subdural hematomas have been reported to occur in 5-25% of patients with severe head injuries, depending on the study. The annual incidence of chronic subdural hematoma has been reported to be 1-5.3 cases per 100,000 population. More recent studies have shown a higher incidence, probably because of better imaging techniques. Sex- and age-related differences in incidence
More common in men than in women, with ratio of approximately 3:1. Men also have a higher incidence of chronic subdural hematoma. The male-to-female ratio has been reported to be 2:1. The incidence of chronic subdural hematoma appears to be highest in the fifth through seventh decades of life. One retrospective study reported that 56% of cases were in patients in their fifth and sixth decades; another study noted that more than half of all cases were seen in patients older than 60 years. The highest incidence, 7.35 cases per 100,000 populations, occurs in adults aged 70-79 years. Adhesions existing in the subdural space are absent at birth and develop with aging; therefore, bilateral subdural hematomas are more common in infants. Interhemispheric subdural hematomas are often associated with child abuse.
Clinical presentation
Acute subdural usually present in the setting of head trauma. This is especially the case in young patients, where they commonly co-exist with cerebral contusions. Most patients (65-80%) present with severely depressed conscious state,
and
pupillary
abnormalities may be seen in 30-50% of cases. Occasionally spontaneous acute
subdural
hematomas are seen with an underlying abnormality (e.g. duralarteriovenous fistula). Clinical presentation of subacute / chronic subdurals in the elderly is often vague and is one of the classic causes of a pseudo-dementia. A history of head trauma is often absent or very minor.
Pathophysiology
Collected blood from the subdural bleed may draw in water due to osmosis, causing it to expand, which may compress brain tissue and cause new bleeds by tearing other blood vessels. The collected blood may even develop its own membrane. In some subdural bleeds, the arachnoid layer of the meninges is torn, and cerebrospinal fluid (CSF) and blood both expand in the intracranial space, increasing pressure
Substances that cause vasoconstriction may be released from the collected material in a subdural hematoma, causing further ischemia under the site by restricting blood flow to the brain. When the brain is denied adequate blood flow, a biochemical cascade known as the ischemic cascade is unleashed, and may ultimately lead to brain cell death. 10 to 30% of chronic subdural hematomas show evidence of repeated hemorrhage. Rebleeding usually occurs from rupture of stretched cortical veins as they cross the enlarged fluid-filled subdural space or from the vascularized neomembrane on the outer (calvarial) side of the fluid collection. Subdural hematomas are interposed between the dura and arachnoid. Typically crescent-shaped, they are usually more extensive than extradural hematomas. In contrast to extradural haemorrhage, SDH is not limited by sutures, but are limited by dural
reflections,
such
as
the falxcerebri, tentorium,
and falxcerebelli. The
body
gradually reabsorbs the clot and replaces it with granulation tissue. Risk Factors
Risk factors for chronic subdural hematoma include the following:
Chronic alcoholism
Epilepsy
Coagulopathy
Arachnoid cysts
Anticoagulant therapy (including aspirin)
Cardiovascular disease (eg, hypertension, arteriosclerosis)
Thrombocytopenia
Diabetes mellitus
In younger patients, alcoholism, thrombocytopenia, coagulation disorders, and oral anticoagulant therapy have been found to be more prevalent. Arachnoid cysts are
more commonly associated with chronic subdural hematoma in patients younger than 40 years. In older patients, cardiovascular disease and arterial hypertension are found to be more prevalent. In one study, 16% of patients with chronic subdural hematomas were on aspirin therapy. Major dehydration is a less commonly associated condition and is found concurrently in only 2% of patients. Causes
(A) Causes of acute subdural hematoma include the following:
Head trauma (fall, motor vehicle collision, assault)
Coagulopathy or medical anticoagulation (eg, warfarin [Coumadin], heparin, hemophilia, liver disease, thrombocytopenia)
Nontraumatic intracranial hemorrhage due to cerebral aneurysm, arteriovenous malformation, or tumor (meningioma or dural metastases)
Postsurgical (craniotomy, CSF shunting)
Intracranial hypotension (eg, after lumbar puncture, lumbar CSF leak, lumboperitoneal shunt, spinal epidural anesthesia [
Child abuse or shaken baby syndrome (in the pediatric age group)
Spontaneous or unknown (rare)
(B) Causes of chronic subdural hematoma include the following:
Head trauma (may be relatively mild, eg, in older individuals with cerebral atrophy)
Acute subdural hematoma, with or without surgical intervention Spontaneous or idiopathic
Signs and Symptoms
Symptoms of subdural hematoma depend mostly on the rate of bleeding:
In head injuries with sudden, severe bleeding causing a subdural hematoma, a person may lose consciousness and enter coma immediately.
A person may appear normal for days after a head injury, but slowly become confused and then unconscious several days later. This results from a slower rate of bleeding, causing a slowly enlarging subdural hematoma.
In very slow-growing subdural hematomas, there may be no noticeable symptoms for more than two weeks after the bleeding starts.
Symptoms of subdural hematoma can include:
A history of recent head injury
Altered breathing patterns
Amnesia Apathy Ataxia, or difficulty walking
Hearing loss or hearing ringing (tinnitus)
Inability to speak or slurred speech
Irritability
Lethargy or excessive drowsiness
Blurred Vision
Loss of appetite
Change in behavior
Loss of consciousness or
Confusion
Deviated gaze or abnormal
Nausea and vomiting
movement of the eyes.
Numbness
Disorientation
Pain
Dizziness
Personality changes
Headache (either constant or
Seizures
fluctuating)
Weakness or lethargy
fluctuating levels of consciousness
Diagnosis
The full extent of the problem may not be completely understood immediately after the injury, but may be revealed with a comprehensive medical evaluation and diagnostic testing. The diagnosis of a head injury is made with a physical examination and diagnostic tests. During the examination, the physician obtains a complete medical history of the patient and family and asks how the injury occurred. Trauma to the head can cause neurological problems and may require further medical follow up. Diagnostic tests may include:
Blood tests
X-ray — a diagnostic test that uses invisible electromagnetic energy beams to produce images of internal tissues, bones, and organs onto film.
Computed tomography scan (Also called a CT or CAT scan.) — a diagnostic imaging procedure that uses a combination of x-rays and computer technology to produce cross-sectional images (often called slices), both horizontally and vertically, of the body. A CT scan shows detailed images of any part of the body, including the bones, muscles, fat, and
organs. CT scans are more detailed than general x-rays.
Electroencephalogram (EEG) — a procedure that records the brain's continuous, electrical activity by means of electrodes attached to the scalp.
Magnetic resonance imaging (MRI) — a diagnostic procedure that uses a combination of large magnets, radiofrequencies, and a computer to produce detailed images of organs and structures within the body.
Treatment
Surgical Management Treatment of subdural hematomas depends on their severity. Treatment can range from watchful waiting to aggressive brain surgery. In small subdural hematomas with mild symptoms, doctors may recommend no specific treatment other than observation. Repeated head imaging tests are often performed to demonstrate the subdural hematoma is improving. More severe or dangerous subdural hematomas require surgery to reduce the pressure on the brain. Surgeons can use various techniques to treat subdural hematomas: 1. Craniotomy Surgery to manage an acute subdural hematoma (SDH) usually consists of a large craniotomy (centered over the thickest portion of the clot) to decompress the brain; to stop any active subdural bleeding; and if indicated, to evacuate intraparenchymal hematoma in the immediate vicinity of the acute subdural hematoma (SDH). A subdural hematoma (SDH) usually has a consistency that is too firm to allow removal through burr holes alone.
Including the sylvian fissure in the craniotomy exposure should be considered, as this is a likely location of a ruptured cortical vessel. If brain injury and edema are associated with the subdural hematoma (SDH), an intracranial pressure (ICP) monitor may need to be placed. Bullock and colleagues stated that "all patients with acute [subdural hematoma] SDH in coma (Glasgow coma scale [GCS] score less than 9) should undergo intracranial pressure monitoring."
Under certain circumstances, craniotomy is recommended for chronic subdural hematoma (SDH), depending on factors such as recurrence, the consistency of the hematoma, and the presence of membranes.
2. Craniectomy
Craniectomy
is
neurosurgical
procedure that involves removing a portion of the skull in order to relieve pressure on the underlying brain. This procedure is typically done in cases where a patient has experienced a very severe brain injury that involves significant amounts of bleeding around the brain or excessive swelling of the brain. Goal
Craniectomy is typically performed as a life saving measure. Patients who have experienced a severe brain injury that is life threatening may have bleeding around their brain or swelling of their brain so severe that it can lead to brain compression and brain death. In this type of dire situation, neurosurgeons can remove a portion of the skull, evacuate any underlying clot that is compressing the brain, and relieve pressure on the brain. Furthermore, because the brain typically experiences a great deal of swelling after a severe injury, removing the bone frees the brain to swell upward rather than downward where it will compress the brainstem, which is critical for all of the basic vital functions, leading to brain death. Over time the brain swelling will subside and the bone that was removed can be replaced. Procedure
Patients with brain injury severe enough to warrant craniectomy are usually already in the hospital and are being monitored very closely. Patients are brought to the operating room, where the anesthesia personnel will continue to closely monitor their vital signs. Meanwhile the neurosurgeons will make an incision in the scalp, typically on the side of the head where the most compression is taking place (especially in cases where the compression is caused by a blood clot). Once the skin and underlying tissues have been cut and moved out of the way, a drill is used to make holes in the skull. The holes are connected with a saw and the bone is removed. Typically the bone is stored in a freezer in hopes that, once the patients’ brain swelling has subsided and their condition is more
stable, the bone may be put back in place. While the bone is removed, patients are provided with a custom fit helmet that they wear to prevent further brain injury. Once the bone is removed, and any bleeding around the brain has been controlled, the skin and connective tissue overlying the brain are closed with sutures. Risks
The major risks of the operation are bleeding and infection and further damage to the brain. As previously stated, patients who require craniectomy as a life saving measure are usually in very critical condition and have in all likelihood already experienced some amount of brain damage. Nevertheless, the surgical team makes every effort to limit the risks of the operation to the patient by administering antibiotics before beginning, controlling all bleed encountered during the surgery, and limiting the amount of manipulation of the brain. 3. Trephination
Liquefied chronic subdural hematomas (SDHs) are commonly treated with drainage through 1 or 2 burr holes. The burr holes are placed so that conversion to a craniotomy is possible, if needed. A closed drainage system is sometimes left in the subdural space for 24-72 hours postoperatively.
Bilateral chronic hematomas (see the following image) may require drainage from both sides, usually during the same operation by means of burr holes placed on each side of the head.
Chronic subdural hematomas (SDHs) are commonly bilateral and have areas of acute bleeding, which result in heterogeneous densities. Note the lack of midline shift due to the presence of bilateral hematomas.
4. Twist Drill Craniotomy
A relatively new system, the Subdural Evacuating Port System (SEPS), was introduced in the mid-2000s, with initial encouraging results. In 2010, Kenning et al and Rughani et al published their results in using this system to treat subdural hematomas (SDHs).
Kenning et al found that SEPS was not only safe and effective in the treatment of subacute and chronic subdural hematomas (SDHs) but that it would be
ideal for patients unable to tolerate general anesthesia (eg, elderly, sick patients) . In addition, SEPS was more effective in draining subdural hematomas (SDHs) that were hypodense on computed tomography (CT) scans than it was in evacuating mixed-density SDHs. Although 1 patient required urgent surgical subdural collection evacuation following iatrogenic injury, Kenning et al noted that significant bleeding was uncommon with SEPS insertion.
Rughani et al reported that SEPS treatment for chronic subdural hematoma had a similar efficacy and safety compared to other twist-drill methods, and its efficacy was also statistically similar to trephination (burr hole), as measured by radiographic worsening or for need for another procedure.There was a trend toward higher recurrence using SEPS but no difference in mortality or other adverse outcomes.
Medical Management
Diuretics
Steroids
Anticonvulsant medicine
Other Management
In cases of severe trauma, immobilize the cervical spine and alert the trauma team. Assessed and manage 'Airway, Breathing and Circulation'. Intubation and assisted ventilation may be needed depending on the level of consciousness. Obtain senior A&E, anaesthetic or neurosurgical advice.
Priority should also be given to obtaining imaging of the head.
Stabilize the patient before transfer for any imaging and send an appropriately experienced member of staff to accompany them during investigations in case of deterioration.
If the condition is strongly suspected or confirmed by investigation, refer urgently to the neurosurgical team.
Mannitol may be considered if there is raised intracranial pressure.
Burr holes may be considered if there is rapid deterioration.
Any coagulopathy also needs treating. If transfer to another site for surgery is necessary, ensure that the patient's condition is optimized and stable before transfer and send an appropriately experienced member of staff, who has the ability to intubate and safely manage the patient in transfer, in case of deterioration.
If there is a small, asymptomatic, acute SDH, this can be managed by observation, serial examinations, and serial CT scanning.
Surgery is needed if there are focal signs, deterioration, a large haematoma, raised intracranial pressure or midline shift.
SDH is treated by emergency craniotomy and clot evacuation.
Recurrence is found in 5-30% of patients, which can be reduced with the use of a drain.
Complications
Death due to cerebellar herniation.
Raised intracranial pressure.
Cerebral edema.
Recurrent hematoma formation during recovery.
Seizures.
Wound infection, subdural empyema, meningitis.
Permanent neurological or cognitive deficit due to pressure effects on the brain.
Coma/persistent vegetative state.
Nursing Care and Management
Monitor LOC using Glasgow Coma Scale (or other objective scale) Assess motor response (bilaterally) Check for positive Babinski’s sign Assess sensory responses (place emphasis on side opposite of injury) Include the following in assessment of pupils: Comparing pupil size, shape and equality bilaterally Check pupils with the direct light reflex (check each eye individually) Check that pupils are equal, round reactive to light accommodation (PERRLA) Assess 6 cardinal fields of gaze (Cranial Nerves 3, 4 and 6) Assess for Doll’s eye phenomenon in unconscious patients (indicates brain stem damage) Monitor vital signs (Notify MD for deviation from set parameters) Provide nursing measures r/t respiratory care including: Suctioning ABG’s Providing O2 Monitoring O2 saturation Monitoring ventilator settings Position pt to maintain venous outflow from brain Elevate HOB to 30 degrees (except for dural tear) No pillow under head (can interfere with venous flow) Turn by logrolling q 2 hrs Administer prescribed medications
Control noise and stimuli Provide rest/activity balance (stagger tasks) Maintain desired temperature range (use antipyretics or hypothermia blanket) Provide nursing care to prevent damage to eyes, skin, oral mucous Provide education and emotional support to family
Nursing Diagnosis
Altered tissue perfusion r/t impaired cerebral circulation Altered sensory perception Impaired gas exchange Self-care deficits Altered body image Potential for skin breakdown Potential for injury Ineffective coping (family) Knowledge deficit Anxiety (fear) Altered Nutrition
Major Goals
Maintain normal ICP Vital signs and ABG’s normal for patient Improvement in LOC
Prognosis
The mortality associated with acute subdural hematoma has been reported to range from 36-79%. Many survivors do not regain previous levels of functioning, especially after an acute subdural hematoma severe enough to require surgical drainage. Favorable outcome rates after acute subdural hematoma range from 14-40%. Several series have shown an increase in favorable outcome in younger patients. Age younger than 40 years was associated with a mortality rate of 20%, whereas age 40 80 years was associated with a mortality rate of 65%. Age older than 80 years carried a mortality rate of 88%. Ultimate prognosis is related to the amount of associated direct brain damage and the damage resulting from the mass effect of the hematoma. Simple acute subdural hematoma (ie, without parenchymal injury) accounts for about half of all cases and is associated with a mortality rate of about 20%. Complicated subdural hematoma (eg, with accompanying contusion or laceration of a cerebral hemisphere) is associated with a mortality rate of about 60%.
Findings on CT scan or MRI may help indicate prognosis. Such findings may include the following:
Thickness or volume of the hematoma
Degree of midline shift
Presence of associated traumatic intra parenchymal lesions
Compression of the brainstem or basal cisterns
The first CT scan may underestimate the size of parenchymal contusions.
In general, a poor preoperative neurologic status may be a harbinger of a poor outcome. In addition to factors discussed above, poor prognostic indicators for acute subdural hematoma have been reported to include the following:
Low initial (< 8) and post resuscitation (< 8) Glasgow coma scale
Low Glasgow coma scale motor score on admission (< 5)
Pupillary abnormalities
Alcohol use
Injury by motorcycle accident
Ischemic damage
Hypoxia or hypotension
Difficulty in controlling ICP
Elevated ICP postoperatively indicates a poor prognosis and may indicate the severity of the underlying brain injury (eg, trauma, secondary infarction).
IV.
CASE STUDY PROPER
A.
PATIENT’S DATA
Medical Case Number:
31028
Department:
Neuro Critical Care Unit
Room Number:
NCCU 5
Name:
Patient X
Age:
87 years old
Gender:
Male
Birthday:
January 17, 1926
Height:
5’2”
Weight:
52 kg
Attending Doctor:
Dr. Jason L. Letran
Admitting Date:
April 27, 2013
Chief Complaint:
Loss of consciousness, poor appetite, and increase somnolence
Admitting Diagnosis:
Electrolyte imbalance
Final Diagnosis:
Subdural Hematoma with Subacute Component
Surgical Intervention:
Bilateral Silver Collar Craniectomy (Surgical Decompression)
B.
PHYSICAL ASSESSMENT
General Survey
An 87 year old man, pale and weak in appearance, afebrile, in light comatose state, in critical condition.
With Endotracheal Mechanical Ventilator
With IV line on left and right upper extremities
Vital Signs
Temperature
36.0C
Heart Rate
67 beats/ minute
Respiratory Rate
14 breaths/minute
Blood Pressure
150/80 mmHg
O2 saturation:
100%
Neurological status
Orientation: GCS 7 (Eyes 2, Verbal 1, Motor 4)
In light comatose state (Inconsistent to painful stimuli, No activity, Purposeful movement varies)
Pain tolerance: sedated
Skin
Fair complexion
With slightly poor skin turgor
Hair
Gray to whitish in color
With evenly distributed hair
No lice or infestation noted
Head
Symmetrical
With Bilateral silver collar craniectomy
Dressing dry and intact
With Jacksons pratt drainage draining 50cc serosanguineous fluid
Can move upon pain stimulation
Symmetrical facial movement
Eyes
With whitish sclera and pinkish conjunctiva
Eyebrows evenly distributed and aligned
Eyelids skin intact, no discharges, no discoloration
Open upon pain stimulation
Pupil of right eye round and reactive to light accommodation
Pupil of left eye round but non reactive to light accommodation
No lacrimation; itchiness and redness
Ears
Auricles color same as face
Auricles are firm non tender and symmetrical
In line with outer canthus of the eye
Pinna recoils after it is folded
No tinnitus, discharges and deformities noted
Nose
No signs of epistaxis
Negative for any discharges
With nasal flaring noted
Nasal septum intact and on midline, symmetrical
No redness or swelling in nasal mucosa
With NGT inserted at left nostril
Mouth
With pale red and dry lips
No lacerations and bleeding ums
No foul breath noted
With Endotracheal tube connected to mechanical ventilator
Neck
Head centered
No palpable mass or lymph noted
Respiratory Status
With symmetrical chest expansion
With clear breath sounds
None chest tubes
Cardiovascular Status
Rhythm: Sinus rhythm
Heart: No murmur
None edema
Pulse palpable and equal
With IV line on left and right peripheral
IV appearance both patent with backflow
Abdomen and Genitourinary
With soft and non-tender abdomen
With hypoactive bowel sounds; with 4-5 bowel sounds per minute
With foley catheter connected to urine bag draining yellowish in color, moderate in amount
Extremities
With immobility of upper left extremities
Can do flexion and extension of upper right extremities
Lower extremities withdrawn to pain; with involuntary movement
With short finger nails; With capillary refill time of 1-2 seconds upon blanching
C. HISTORY OF PRESENT ILLNESS
History of present illness started last Thursday April 25, 2013. The patient together with his caregiver went to park and stroll there. The caregiver observed that the patient seems tired but they still continue to walk and travel to reach their destination. Then the next day the patient reports of body weakness, loss of appetite, and the caregiver observed that the patient have increased time of sleep.
Then on Saturday , April 27, 2013 the patient didn’t woke up upon awake ning of his caregiver. The family decided to bring him to Cardinal Santos Medical Center. The initial diagnosis was electrolyte imbalance, and after conducting different laboratory ad diagnostics the patient was diagnosed with subdural hematoma. The client underwent surgical intervention of bilateral silver collar craniectomy (Surgical decompression) on April 28, 2013.
D. PAST MEDICAL HISTORY On January 2013, the patient was diagnosed with benign prostatic hyperplasia and underwent surgery. The patient suffers from hypertension and have maintenance drug.
E. FAMILY HISTORY The family of the patient has history of hypertension, yet no known diabetes mellitus, asthma, cancer and other disease. The family has no any other history of hospitalization.
F. SOCIAL/PERSONAL HISTORY The patient even though he’s old age still time to talk with his friend and often travels. He is always accompanied by his caregiver wherever he went.
G. FUNCTIONAL HISTORY Patient can perform activities of daily living yet sometimes need caregiver to do some tasks prior to his illness.
V.
LABORATORY RESULTS
1. ECG Result
April 29, 2013
Sinus rhythm and premature ventricular complexes or fusion complexes Left ventricular hypertrophy With repolarization abnormality Prolonged QT Abnormal ECG
2. 2D echo (2 Dimensional Echocardiogram)
April 27, 2013
Concentric left ventricular hypertrophy with left ventricular mass index of 126.23gm/m 3 and relative wall thickness of 0.40 with moderate hypokalemia of the interior left ventricular free wall from the base to apex and mild hypokalemia of the anterior and antero-lateral ventricular free wall from base to apex Mitral stenosis with mitral regurgitation; moderate Aortic sclerosis with aortic regurgitation; moderate Tricuspid regurgitation; mild Mild pulmonary hypertension with pulmonary regurgitation; moderate Interatrialseptal aneurysm
Nursing Responsibilities: Assessed contributing factors such as lifestyle Monitored vital signs esp. BP Encouraged to avoid strenuous activities Emphasized importance of having adequate rest and sleep periods Administered medications as ordered
April 27, 2013
3. Liver Function Tests
Component
SGPT/ ALT
Normal Values
8.00 – 53.00 u/L
Result
29.00 u/L
Interpretation
Within Normal Values
Nursing Responsibilities: Encouraged to maintain balanced CHO, CHON and fats diet Emphasized importance of limitation of fatty and salty foods Stressed to limit/avoid alcohol drinking
4. Arterial Blood Gas (Blood Gas Values) Component
pH pCO2 pO2 HCO3
April 30, 2013
Normal Values
7.35- 7.45 35-45 mmHg 80- 100 mmHg 22-26mmol/L
Result
7.445 31.0 mmHg 220.7mmHg 20.9 mmol/L
Interpretation
Respiratory Alkalosis complete compensation
Related Nursing Care: Arterial blood is collected in a heparinized needle and syringe Sample is placed on an icebag and taken immediately to the lab If client is receiving oxygen, indicate on lab slip Apply pressure on puncture site for 2-5 minutes or longer if needed Do not collect blood from the same arm used for an IV infusion Nursing Responsibilities:
Assessed respiratory rate, depth and ease. Monitored vital signs and skin color Protect the client from injury by raising side rails and providing restraints Monitor and adjust the mechanical ventilator as needed Frequently check ABG result for improvement
5. PTT-Prothrombin Time Component
Normal Values
April 28, 2013 Patient value
Control
Interpretation
PTT
28-44.0
36.5
32.2
Within normal values
Prothrombin Time
9.5 – 12sec
14.0 sec
12.3 sec
Within normal values
Activity
<61.5 %
INR
1.17
Nursing Responsibilities:
Assessed the general condition of the patient Monitor capillary refill Monitor vital signs esp. BP for narrow pulse pressure Encouraged patient to increase oral fluid intake Checked patient for bleeding
6. Electrolyte Values (Sodium, Potassium, Ionized Calcium, Magnesium) Component
Normal Values
Result
April 27, 2013
Interpretation
Na
135-145 mEq/L
140.90mEq/L
Within normal values
K
3.5 – 5.0 mEq/L
3.16mEq/L
Hypokalemia
Ca
4.5 – 5.5 mg/dl
4.32 mg/dl
Hypocalcemia
Mg
1.5 -2.5 mg/dl
1.85 mg/dl
Within normal values
Nursing Responsibilities: For hypokalemia: Include potassium rich foods in the diet, such as banana, dried fruits, orange, raw carrot, raw tomato, baked potato, melon, ad watermelon. Administer potassium supplement (Potassium Chloride) per slow IV drip. Never administer Potassium Chloride per IV push or Direct IV. This may cause dysrhythmics and cardiac arrest. For hypocalcemia: Encouraged high calcium diet. Oral calcium salts as prescribed. Promote safety. Seizures may occur. Protect from trauma. To prevent fracture. Monitor breathing. Administered oxygen, Larygospasm may occur.
7. X-Ray April 27, 2013 Fibrotic densities are seen at both upper lobes, more on the right probably residual from previous infection The rest on the lung fields show no reactive parenchymal infiltrates Heart is magnified Aorta is tortous and calcified Hemidiaphragms, sinus and soft tissues are intact Note of degenerative changes of thoracic spine
Nursing Responsibilities: Assessed contributing factors such as lifestyle Assessed breathing pattern, characteristics, and sounds Reviewed cholesterol level in the lab results Encouraged the pt. to avoid eating fatty and salty foods Taught to have balanceand eat diet nutritious foods such as green and leafy vegetables, oat meals or cereals, and other soluble fibers Encouraged pt. avoid strenuous activities Emphasized importance of daily exercise
8. CBC (Complete Blood Count) Component
WBC RBC Hgb Hct Platelet
April 29, 2013
Normal Values
Result
Interpretation
5.0 – 10.0 k/ mm 4.5- 5.3 10 /L 13.5 – 18 gm/dl
8.6 k/ mm 4.5 10 /L 15 gm/dl 0.38 % 0.221 10 /L
Within Normal values
0.140-0.440 10^12/L
Diff count Segmenters
55 – 70%
0.83
Increased (with ongoing antibiotic therapy)
Lymphocytes
20 - 40 %
0.12
Decreased (Chronic bacterial infections)
Monocytes
2- 8 %
0.05
Within Normal values
Nursing Responsibilities:
Assessed the general condition of the patient Assessed patient for bleeding Encouraged to include iron-rich and protein-rich foods Provided adequate rest and sleep periods Encouraged to do breathing exercises Administer iron supplement as ordered Reviewed the current laboratory result Re-assessed the patient
9. BUN Creatinine Component
BUN Crea
April 27, 2013 Normal Values
7.00 – 19.00 mg/dl 0.60 – 1.30 mg/dl
Result
Interpretation
12. 53 mg/dl 0.75 mg/dl
Within Normal Values
Nursing Responsibilities: Monitor intake and output Encouraged diet low in sodium and fat like fruits and vegetables such as malunggay and guava Advise to have daily exercise at least 10mins/day Regulate IVF properly Assessed for signs and symptoms of increased creatinine such as urinary frequency. Instructed patient to avoid foods that are rich in salts and fats .
10. Serum Protein Component
April 27, 2013 Normal Values
Result
Interpretation
Protein Total
6.30 – 8.20 g/dl
6.70 g/dl
Within Normal Values
Albumin
3.50- 5.00 g/dl
3.20 g/dl
Decreased (acute/chronic infection Immunologic deficiencies due to aging)
Globulin
2.30 – 3.50 g/dl
3.50 g/dl
Within Normal Values
Nursing Responsibilities: Assessed presence of edema or malnutrition Encouraged patient to take foods rich in protein such as organ meats and egg white
IX. EVALUATION
Subdural Hematoma brought severe suffering to the patient and the family. The disease affects the brain and it parts which make the persons functional and holistic ability deteriorating. Handling patient with subdural hematoma offers advance knowledge regarding neurologic disorders.
Within the week of exposure I was able to see the improvement on the client’s condition. On the first day, the patient was sent to the Intensive Care Unit after the bilateral silver dollar craniectomy due to bilateral subdural hematoma. The patient was in GCS 6 by that time with different contraptions such as mechanical ventilator, and infusion pump. As well as the patient drains serosangious fluid via Jackson ’s pratt. While handling the patient I able to learn how to utilize cardiac monitor, control the mechanical ventilator and the infusion pump. It also provide opportunities such as NGT feeding, draining, suctioning, back tapping, bed making, turning exercises, and vital signs monitoring. It also great opportunity that during the doctor’s round, some of them discussed about client’s case and
further elaborate within the reach of our understanding. As days passed by the client’s condition improved, from GCS 6 to GCS 11. All the diagnostics and laboratory examinations help to determine the clients good progress.
In four days of exposure the student nurse had a great opportunity to enhance his skills, knowledge and attitude. First of all he became more knowledgeable about subdural hematoma specifically about the treatment, nursing management, pathophysiology, and overview of the disease. As well as it also enhance my awareness of the bilateral silver dollar craniectomy and its management. The knowledge helps to provide the necessary care and interventions through history taking and physical assessment. The student nurse was able to formulate nursing care plan and the outcome commendable.
Exposure to patient with Bilateral subdural hematoma with subacute component s/p bilateral silver dollar craniectomy, as well as being exposed with the kind of hospital like Cardinal Santos Medical Center is something to be treasured in the nursing student’s life. I
am thankful to my patient, groupmates, clinical instructors, staff nurses and doctor and other members of health care team which made this duty a memorable and fruitful one.
