Medical Case Study Left Frontal Intraparenchymal Hemorrhages Biology Essay

Chief Ailment: Headache, sickness, and failing. History of Present Illness: 67 twelvemonth old RH adult male with a history of CHF, HTN, lipemia, atrial fibrillation on Coumadin, and CAD s/p CABG on acetylsalicylic acid and clopidogrel bisulfate admitted for subdural bleeding. On 9/16, patient presented to Wall Hospital at 10am with sudden oncoming concern, sickness, and right sided failing. Harmonizing to ER notes, his boy stated at that place may hold been a battle the twenty-four hours before at place but married woman denies this. Patient had ecchymoses on his left arm and upper thigh but no scalp haematoma. His neurological test was important for lassitude, dysarthria, right hemiparesis, and Babinski mark on the right. Head CT showed a big left subdural haematoma with 18mm of midplane displacement. He was given mannitol 50mg, vitamin K 10mg, and FFP. He was intubated and transferred to the NICU at midday.

Hospital Course: On test under propofol, patient did non react to command, open his eyes, or wink to menace ; his students were reactive ; there were no oculus motions with oculocephalic maneuvre ; corneal physiological reaction was present ; and he was retreating bilaterally, left more than right. He was given vitamin K 10mg, DDAVP 24mg, FFP, and thrombocytes, and taken to the OR for exigency decompression. After surgery, he developed self-generated bleedings in the cerebellum and left frontal lobe. Patient continues to hold atrial fibrillation throughout his infirmary class. On 9/17, his PT was 19.2, PTT 32.4, and INR 1.55. Tracheostomy turnup was changed on 9/30. Sputum civilization on 9/29 showed klebsiella pneumoniae and patient was started on Pipracil tazobactam, Nebcin, and Vancocin. Patient continues to hold shudder in his caput, left arm and leg. cEEG on 9/30 showed no ictic beat associated with the shudder. Patient was watchful and able to follow bids yesterday.

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Past Medical History: CHF, HTN, lipemia, atrial fibrillation on Coumadin, CAD s/p CABG in 1999 on acetylsalicylic acid and clopidogrel bisulfate.

Past Surgical History: left hemicraniectomy, external ventricular drain, PEG arrangement, tracheotomy.

Family History: Noncontributory.

Social History: Patient is to the full functional and lives with his married woman. Denies smoke, intoxicant, or drug usage.

Medicines:

Home Medicines:

Lisinopril 20mg PO daily

Hctz 25mg PO daily

Coumadin 4mg PO daily

Lipitor 20mg PO daily

Amlodipine 10mg PO daily

Digoxin 125mg PO daily

Metoprolol 25mg PO daily

Plavix 75mg OP daily

Protonix 40mg PO daily

Aspirin 81mg PO daily

Standing Master of educations:

Piperacillin Tazobactam Inj +R+ 4.5 G IVPB q8hr

Tobramycin Inj 500 MG IVPB q24h

Vancomycin IVPB **INITIAL-72 HR STOP** 1250 milligram IVPB q12hr ( completed )

Digoxin Load Oral Liq 100 mcg PO q24h

Furosemide Oral Liq 40 MG PER PEG q12hr

Lisinopril Oral 20 MG PO q24h

Metoprolol Tartrate Oral 50 milligram PO q6hr

Ipratropium Bromide Inh Soln 2.5 ML INHALATION q6hr

Escitalopram Oral 10 milligram PO q24h

Fentanyl Patch 12 mcg TRANSDERM q72h

Levetiracetam Oral Liq 500 milligram PO q12hr

Enoxaparin Inj 40 MG SUBQ daily 9am

Docusate Sodium Oral Liq 100 MG PER PEG tid- ( 9,13,17 )

Esomeprazole Oral Liq 40 milligram PO daily 9am

Multivitamin Oral Liq 5 ML PER NG bedtime

Senna Oral Liq 10 ML PER NG daily 9am

Acetylcysteine 20 % Inh Soln 3 milliliter INHALATION q12hr

Chlorhexidine Gluconate Oral Soln 15 milliliter SWAB q12hr

free H2O 250 milliliter PER PEG q6hr

Nystatin Topical Powder 1 APPLIC TOP q8hr

PRN MEDS:

Acetaminophen Oral 650 milligram PO q4h

Acetaminophen Rectal 650 MG RECTAL q6hr

Oxycodone Immediate Release Oral 5 MG PER PEG q4h

Oxycodone Immediate Release Oral 10 MG PER PEG q4h

Fleet Enema Adult Rectal 1 UNIT RECTAL Once

Allergies: Cefazolin induces hives..

Physical Examination:

VITALS ( last 24h ) :

Technetium: 37.9 Tmax: 38.4 @ 02 Oct 20:00

Hour: 86 ( 80 – 116 )

BP: 136/90 ( 131/77 – 156/99 )

Manner: Vol Contl, FiO2: 40, SpO2: 98 % ( 92 – 98 ) , RR ( set ) : 12, VT ( set ) : 550, VT ( exhaled ) : 575, MV ( exhaled ) : 9.5, PEEP: 5

General: Liing in bed with shudder in left arm and leg.

HEENT: Tracheostomy site clean and dry.

Skin: No roseolas.

Cardiac: Irregularly irregular beat. Normal S1 and S2. No carotid bruits.

Pneumonic: Lungs clear to auscultation.

Abdomens: Normal intestine sounds. Not distended and no multitudes. PEG site clean and dry.

Extremities: 3+ bilateral opposing hydrops. 3+ biceps, radial, dorsalis pedis pulsations. 0+ popliteal and posterior tibial pulsations.

Guam: Urinating via texas catheter.

Neurological:

MSE: Opens eyes in response to verbal bid and spontaneously. Can lodge out lingua on bid but does non react to other bids. Can non reply inquiries verbally. Paths motion with eyes.

Cranial nervousnesss: PERRLA 3- & A ; gt ; 2.5mm. Tongue protrudes symmetrically.

Motor: Normal majority. Flaccid appendages on right. Normal tone on left. No opposition to fall on either arm. Moves left upper arm spontaneously but non other limbs.

Sensory: Extremities withdraw to trouble.

Reflexs: 2+ biceps, triceps, brachioradialis, patellar, and Achilles tendon physiological reactions bilaterally. No clonus or Babinski marks.

Coordination: Not tested.

Pace: Not tested.

LABS ( last 24h ) :

145 | 102 | 36

— — — — — — — — — — & A ; lt ; 135 Ca: 8.2 Phosphorus: 4.6 Mg: 2.3 [ 10/03 @ 05:00 ]

4.2 | 28 | 2.2

Leukocyte: 14.1 / Hb: 8.6 / Hct: 30.3 / Plt: 314 [ 10/03 @ 05:00 ]

Imagination:

MRI encephalon ( 9/22 ) : Persistent bilateral excess axial aggregations left larger than right, left associated with postop alterations and some minimum mass consequence no midplane switch the ventricular size is unchanged since anterior CT scan, little country of acute infarct in the left posterior frontal cerebral mantle

CT caput ( 9/19 ) : Interval minimum expansion of the left frontal extra-axial aggregation underneath the bony flap as described when compared to the earlier scan otherwise ventricular size is stable. Increase in size of left frontal parenchymal bleeding with increased mass consequence upon the left frontal horn and mild left-to-right midplane displacement.

CT caput ( 9/19 ) : Little lessening in hydrocephaly, no alteration in bilateral cerebellar bleedings with relentless mass consequence upon the 4th ventricle, new left frontal deep white affair parenchymal bleeding sidelong to the left frontal horn

CT caput ( 9/17 ) : New interval little inward supplanting of the left craniotomy bone fragment, relentless bilateral cerebellar and left inferior frontal bleedings, stable, interval lessening in pneumocephalus, ventricular size is stable with relentless mild distension of the temporal horns, relentless tentorial bleeding, s/p drain arrangement, postsurgical alterations with 8mm left-to-right midplane displacement secondary to left frontal lobe swelling

CT caput instantly post-craniectomy ( 9/16 ) : Diffuse intellectual swelling with effacement of the basal cisterns and 4th ventricle, thin residuary left posterior interhemispheric subdural bleeding, without important mass consequence, no acute big infarct.

Neurophysiology: 9/30 cEEG:

1. Background: Continuous and reactive. 2. There was uninterrupted focal deceleration in the left hemisphere, maximum left temporal, chiefly in the delta scope. 3. No epileptiform discharges. 4. There were frequent periods of intermittent irregular leftward caput jolt and left shoulder jolt. These were non associated with any definite ictic beat on EEG. 5. Sleep: State alterations but no normal phase 2 sleep transients.

Echocardiogram: TTE: Very limited survey, normal LV and RV size and map – clear regional wall gesture abnormalcies are non seen, important valve disease is non seen, trace pericardiac gush.

Appraisal: 67 twelvemonth old adult male transferred from Palisade Hospital for left subdural bleeding while on anticoagulation and antiplatelet medicines, s/p left hemicraniectomy with subsequent bilateral cerebellar and left frontal intraparenchymal bleedings, clogging hydrocephaly s/p external ventricular drain, s/p tracheotomy and PEG arrangement, now with continued altered mental position including decreased watchfulness and attending.

Localization: At the clip of initial presentation to Palisades Hospital, the patient ‘s symptoms of concern, dysarthria, and lethargy suggested increased intracranial force per unit area. His right hemiparesis and right Babinski mark suggested a big, left sided lesion affecting the motor cerebral mantle. Presently at CUMC, the patient ‘s altered mental position suggests a CNS lesion. Paralysis of the patient ‘s right arm and leg suggest a left frontal lobe lesion while palsy of the left leg suggests a right frontlet lobe lesion that is parafalcine. The one lesion that can explicate both findings is an interhemispheric subdural bleeding.

Subdural haematoma ( SDH ) is a bleed into the subdural infinite between the dura mater and arachnidian mater. The most common causes are head injury, intellectual wasting, and antithrombotic therapy. In this instance, the patient ‘s SDH may hold been caused by a combination of all three. First, there is a possible history of caput injury on the dark prior to the oncoming of symptoms. Head injury, such as falls, motor vehicle accidents, or assaults, can take to tear of the bridging veins that drain into the dural fistulas or the rupture of little cortical arterias ( Gennarelli 1982 ) . Second, given the patient ‘s age, he is at increased hazard for intellectual wasting. Two other hazard factors for intellectual wasting, neither of which the patient has, are alcohol maltreatment and old traumatic encephalon hurt. Third, the patient was on the anticoagulant Coumadin and the antiplatelet agents aspirin and clopidogrel bisulfate when his symptoms began. Surveies have shown that antithrombotic agents increase the hazard for SDH. Indeed, one survey of patients with chronic SDH following caput injury showed that 21 % had been on unwritten decoagulants and 13 % on acetylsalicylic acid at the clip of bleeding ( Reymond 1992 ) .

This patient ‘s SDH can be classified as ague based on the fact that he experienced rapid neurological diminution within one to two yearss of oncoming of symptoms. Half of patients with acute SDH enter a coma at the clip of hurt. However, in 12-38 per centum of instances, including this patient, there is a limpid interval following hurt before the patient descends into a coma ( McBride 2010 ) . In add-on to the history and physical test findings outlined above, imaging is an of import subscriber to the diagnosing of SDH. The imaging mode used in this instance was head CT, which has the advantages of velocity and cost over encephalon MRI. On CT, SDH is visualized as a crescent shaped country of hyperdensity. However, encephalon MRI is more sensitive for SDH than CT, particularly for interhemispheric SDH ‘s as was the instance in this patient.

An of import direction determination in acute SDH is whether to surgically evacuate the haematoma or pull off it nonsurgically. Current recommendations propose that an acute SDH with a thickness of greater than 10mm or a midline displacement greater than 5mm on CT should be surgically evacuated regardless of the patient ‘s Glasgow Coma Scale mark ( Bullock 2010 ) . Given that this patient had a terrible midplane displacement of 18mm, surgery was the right direction pick. Surgical options include burr hole trephination and decompressive craniectomy. There is limited informations to propose that craniectomy produces superior results to burr hole trephination ( Chesnut 2006 ) . The patient was rushed to the OR shortly after admittance because surveies have shown that surgery performed within 2-4 hours after oncoming of symptoms produced lower morbidity and mortality compared to detain surgeries ( Haselsberger 1988 ) .

In order for the surgery to take topographic point, the patient ‘s antiplatelet and anticoagulation medicines were stopped and reversed. Current options for change by reversaling anticoagulation include fresh frozen plasma, factor II complex dressed ore ( PCC ) , recombinant human factor VIIa and vitamin K. In this instance, fresh frozen plasma and vitamin K were used because of their handiness. However, PCC when available is recommended over FFP because it provides all of the vitamin-K dependent curdling factors in a smaller volume ( McBride 2010 ) . DDAVP and thrombocytes were besides given to the patient to advance primary haemostasis. Intravenous Osmitrol was given to cut down the patient ‘s elevated intracranial force per unit area.

Plan:

Neurological

1. Monitor neurological test and repetition caput CT to measure for bleedings or hydrocephaly.

2. Continue Keppra 500mg PO BID for ictus prophylaxis.

3. Continue PT/OT and buttocks for temperament to acute rehabilitation.

4. Neurosurgery is following sing skull flap replacing.

5. Continue lexapro for depression intervention.

6. Oxycodone PRN and fentanyl spot for hurting.

Cardiovascular

1. Lisinopril and furosemide to command blood force per unit area. Target SBP & A ; lt ; 130.

2. Digoxin and Lopressor for rate control for atrial fibrillation.

3. Telemetry.

Pneumonic

1. Continue A/C airing.

2. Continue ipratropium and acetylcysteine.

Gilbert

1. PEG placed 9/28.

2. Esomeprazole.

3. Senna and docusate.

Nephritic

1. Free H2O 250cc per PEG q6hr.

2. NS 1000ml IV 20ml/hr to rectify elevated BUN.

Infectious Disease

1. Continue Vancocin, Nebcin, and zosyn ( started 9/30 ) for klebsiella pneumonia.

2. Monitor Tobramycin and vancomycin trough.

3. Nystatin pulverization to go forth armpit.

4. Follow up blood and urine civilization, C. difficile PCR.

5. Acetaminophen for febrility.

Heme

1. DVT prophylaxis: Venodyne boots and lovenox.

2. Monitor INR. Goal & A ; lt ; 1.4.