Ruby Cerdeño 2014A SUBJECTIVE DATA: Pertinent (+) The patient is a right handed, non-hypertensive/non-diabetic 51 y.o.

male who presented with generalized headache of three hours duration. He had history of head trauma two days prior to admission wherein he contracted an ecchymosis on the left eye. His left face, including left upper and lower lip, were swollen and ecchymotic. Patient also had a hematoma on frontal and occipital area and vomited hours after. He was then admitted to San Jaun De dios where he was given Vitamin B12 IM and was then ransferred to Manila Doctor’s Hospital. Upon assessment, initially, patient can follow commands, ambulatory, with good urine output but hours after admission, patient’s condition deteriorated (verbal output is only ‘yes’ or ‘no’). He was given ceftriaxone, Mannitol, Ompeprzole. Upon admission to UERM, patient is still responsive.

Dr. Tan

Pertinent (-) Patient did not present with headache. He did not have history of dizziness, blurring of vision, weakness, numbness, and there is no history of loss of consciousness.

OBJECTIVE DATA: Pertinent (+) Physical Examination  Patient is stuporous  The left side of his head was wrapped in bandage and with JP drain  His occipital area with a 2-inch healing laceration  Left eye was swollen, with purplish discoloration of areas surrounding the eye; Left eye was bloodshot, with subconjunctival hemorrhage noted on the lateral aspect  Right eye was not swollen, but area under the right eye also has a purplish discoloration; No redness or exudates present on right eye  Left ear canal was filled with blood crusts  Left side of the lips were notably swollen with a dark discoloration Neurological Examination  Stuporous but arousable by vigorous tapping  Slightly Responsive to verbal command (shake or nod head to yes/no questions)  GCS Score: 11 [Eye: 4 (spontaneous opening); Verbal: 2 (comprehensible sound); Motor: 5 (point locally to pain]  Weakness on all extremities except right upper extremities ASSESSMENT: Localizing the Lesion: Subarachnoid Patient was well until two days prior to admission when he sustained head injury after a fight. The patient developed ecchymosis on his left face which was also swollen. On the same day, the patient complained of headache and had a single episode of vomiting hence he was brought to hospital. Upon assessment, patient can still follow commands, ambulatory, has good urine output but patient’s condition deteriorted untill the point wherein his verbal output only ‘yes’ or ‘no’. He was then brought to the UERMMCI wherein he was still responsive by to but by only shaking or nodding his head to yes or no question. Upon physical examination, aside from his lacerations/ecchymosis and low Glasgow Coma scale (11 = moderate head injury), the patient was also observed to have weakness on all his extremities except for his right arms. Pertinent (-)  Not in respiratory distress  No nasal flaring  No numbness, hypo/hyperreflexia

often irreversible. Thus when the patient is “at risk. may also be ruled out. and the subsequent precise rate of blood accumulation within the epidural space. precipitating hip flexion. coma develop within just 1 hour after the blunt head injury. Examination of the optic fundi frequently discloses retinal or preretinal hemorrhage. subdural hematoma. their etiology. and is frequently associated with pain extending across the head and toward the neck. Terson syndrome is a frequent cause of visual loss in SAH. with a constant viselike ache but occasionally throbbing. it could be inferred that he may have has sustained a hemorrhage which may present as epidural hematoma. associated with nuchal rigidity. generalized headache. may be rule out since 1) there was no loss of consciousness and 2) there was no rapid progression to coma. The actual rate of symptom progression depends on the type of associated brain injuries. and hamstring pain. During the moment of rupture. emergency surgical evacuation is indicated. Subsequently. even fleetingly. aside from his lacerations and hematoma. to transient loss of consciousness. subarachnoid hemorrahage. However. to altered mental states. and altered consciousness are often associated with the headache which was presented by the patient. Brudzinski’s maneuver is an excellent means of evaluating meningismus. Unfortunately. the examiner flexes the patient’s neck. Seizure-like activity may be observed. Seizures in SAH are most commonly associated with middle cerebral artery (MCA) and anterior communicating artery (ACA) aneurysmal rupture causing intracerebral hematomas. however. as the torn vessels leak. knee flexion. the patient ‘typically’ experiences an initial but relatively brief loss of consciousness secondary to th e primary concussive injury. The headache is usually global. he only presented with altered mental status. subdural hematoma. an epidural hematoma develops and enlarges. one fourth of patients become comatose and up to 40% have transient loss of consciousness. In the case of the patient. Any failure to recognize an epidural . This headache is somewhat milder and usually not associated with meningismus. Unilateral aches or a retro-orbital stab-like pain. The initial severity of the injury determines the patient’s clinical presentation. Hemorrhage into the vitreous results in Terson syndrome. this varies from neurologically intact. many patients recall having a sentinel hemorrhage or warning leak with a fleeting but severe headache within the 2–3 weeks before the major ictus. This may show induration mainly of blood vessels near the injury (medial left side) which may have had eventually involved the left cranium as it pass through the falx cerebri. a vitrectomy is occasionally required. The headache peaks rapidly. subsequently associated with pupillary inequality and motor weakness. as seen in the patient. Its association with ACA aneurysms is less clear. is also commonly seen with acute SDH which was not seen in the patient. When evaluating patients with SAH or sudden severe headache. Diplopia (due to abducens or oculomotor nerve palsies) and visual loss (chiasmal or optic nerve involvement) are caused by either cranial nerve compression from the aneurysmal dome or aneurysmal rupture and increased intracranial pressure.” only to have a devastating.With the patient’s history of head injury. and eventually becoming comatose with signs of decorticate or decerebrate posturing. the initial CT is normal as the hematoma has yet to develop to a size that is definable. This presentation supports the inference that the patient may have had developed subarachnoid hemorrhage. It is often related with more severe subarachnoid bleeds that cause loss of consciousness and papilledema. The long-term prognosis for vision in this situation is fairly good. subhyaloid hemorrhages. excruciating and unbearable. On occasion. together with his presenting signs and symptoms (as mentioned above). Once the EH is identified. In epidural hematoma. This is then followed by a lucid interval with return of wakefulness. after the closed head injury. special attention should be focused on the level of consciousness. it is often ignored until the catastrophic return of a major rupture. and to a brief period of a “paradoxically reassuring alertness. Approximately 30% of patients are found to be confused and lethargic after the ictus.” Headaches associated with aneurysm rupture are frequently s udden in onset and often described as a severe thunderclap. biconvex collection between the skull and brain. Primary Impression: Subarachnoid hemorrhage Secondary to Trauma PLAN: Diagnostics  Electrodiagnostic studies: CT scan with angiography repeatedly to follow extent/progression of brain injury o Epidrual Hematoma: Cranial CT imaging usually demonstrates a hyperdense.” it is essential to be prepared to repeat the CT scan at the slighte st change in clinical status. with scarring and epiretinal membrane formation (macular pucker) and eventually visual loss or distortion. a classical finding with epidural hematoma. Nausea and vomiting. Though patient presented with altered mental status.. neck pain. leading to a rapid lapse into coma. and signs of meningismus. which usually involves the middle meningeal artery or arteries perpendicular to the fracture. which often goes unnoticed until the patient regains consciousness 1–2 weeks later. this classic presentation occurs in less than one third of affected individuals. Sometimes this entire process may transpire from injury. The incidence of true seizure activity in patients with SAH is estimated at 20%. and weakness of all the extremities except for the right upper arm. The lucid interval. The classic symptom of SAH is the “worst headache of one’s life. raise the suspicion of a possible posterior communicating artery aneurysm. focal neurologic signs such as hemiparesis or cranial nerve palsies. Epidural hematoma. Meningismus frequently occurs. and occasional papilledema. It may be possible that structures in the t lateral side was spared hence sparing his right upper extremities.

When the presence of blood in the CSF does not clear between the first and fourth tubes. and often persists for approximately 2 –3 weeks. When SAH is confirmed by CT or lumbar puncture. a repeat study should be performed approximately 10 days later. intraventricular hemorrhage. Unlike epidural hematomas. An aneurysmal source is found in 80–85% of arteriograms preformed for suspected SAH.  Manage elevted intracranial pressure using mannitol 20-50g in 20% solution. A nontraumatic tap is crucial. the cause of the hemorrhage is best evaluated with a four-vessel cerebral arteriogram. Whenever the clinical suspicion of SAH exists but CT is negative. If arteriography is negative after SAH. hematoma size. aspiration pneumonia. time of treatment. and sometimes extend along the falx cerebri. or subdural hemorrhage. An acute SDH is recognized by its hyperdense crescent-shaped image between the brain and skull . CT confirms the presence of SAH and frequently highlights associated issues such as hydrocephalus. Head CT sometimes underestimates the size of the SDH given the similar imaging density of the nearby bone. glucose-thiamine may be used.  Lumbar puncture: if subarachnoid hemorrhage is suspected Management  Establish clear airway for oxygen delivery  Manage shock. drug intoxication. Its sensitivity is highest in the first 24 hours after headache onset. a more sensitive indicator is CSF xanthochromia. Although reliance on CT angiography rather than catheter angiography has been increasing. 57-7). Subarachnoid Hemorrhage: The clinical diagnosis of SAH is best confirmed with brain CT (Fig. If diagnosis is unknown.  Indwelling catheter should be placed  In severe hyperthermia. this is particularly suggestive of SAH (See Fig. However. which represents lysis of erythrocytes with degradation of heme products into bilirubin within the CSF. cerebral arteriography remains the accepted standard for evaluating patients with SAH. 57-5). infusied via IV in 10-20 minutes. evaporative cooling mechanisms and antipyretics are advisable  Prevention of gastric hemorrhage. Subdural Hematoma: Brain CT is the initial test of choice for detecting SDH and concomitant brain injuries.o o hematoma has a most significant mortality depending on patient age. It can also be used for supplementation of nutrients. excessive gastric secretion. This frequently renders the CSF a yellowish color within 1–3 hours after an SAH. and only one third are seen after 2 weeks. if present  IV line establishment for determination of glucose level. a lumbar puncture must be performed. intraparenchymal hematoma. A mild hemorrhage may wash away within 24 hours but approximately 50% of severe SAHs are still visible on CT 1 week after the ictus. a combination of naloxone. leg vein thrombosis. kidney and liver function tests. and associated injuries.  Regular lubrication of the conjunctiva and oral hygiene . SDHs typically cross skull suture lines.

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