Case Studies for Nursing Students - Nursing Case Studies
DetailsClinical Significance/ImpactHistory of present illness: Susan Simmon is a 30-year-old Asian female who was transported by ambulance. Her spouse is at bedside. Upon admission to the emergency department (ED) at 20:22, she was following commands, and c/o a severe headache with a pain level of 7 out of 10, tingling and weakness in left arm, dizziness and nausea.Severe headachePainTingling & weakness left armDizzinessNauseaSocial History (from Susan and Spouse): Susan lives with her spouse of four years. They have no children and no pets in the home. She works for a large investment banking firm and was recently promoted and transferred to a new location. Occupation and living conditions do not suggest potential exposure to pathogens, contaminants or toxins. Spouse not experiencing any symptoms.Medical History: No significant medical HxFamily History:Patient states that her mother had migraines and died at the age of 70 after a heart attack. Her maternal grandfather had a stroke at age 69. There is no other family history of stroke or vascular disease, but she has no information about her father’s side of the family.Family hx suggests that the patient is at a higher risk of heart attack or stroke (Tischler, 2017).Family hx of migraine headaches. Current Medications:Estrostep FeMultivitaminAllergies:NKDAUse of Estrostep Fe does not suggest a higher than average risk of stroke or heart attack. Pt. Is not over 35 yo, is neg. for risk factors and is a nonsmoker (PDR, 2018).Subjective History (Spouse):Spouse states that since Susan was promoted, she has been working far more hours away from home. She is easily agitated and has had difficulty sleeping. Upon arriving home this evening, she c/o fatigue and a severe headache. Minutes later, her spouse found her on the bedroom floor with left sided weakness plus urinary incontinence and called for emergency services.Spouse states patient has exhibited signs ofIncreased stressChanges in moodDifficulty sleepingObjective DataGeneral Appearance: Pt is supine in bed, head elevated 30 degrees, c/o severe headache and nausea. Pt is diaphoretic.VS: Temp: 36.5℃ (97.7℉ BP: 156/88HR: 90RR: 22Ht: 63 inchesWt: 125lbs & 56.8kgRESP: O2 Sat. is 98% on 3 liters/min nasal cannula. Lungs CTA B. No RRS observed.CARDIAC: Regular heart rate with normal S1 and S2. No appreciable murmurs, rubs or gallops.NEURO: Glasgow Coma Scale is 15, opens eyes to voice (E4), oriented to person, place and date (V5), dense left hemiparesis but able to move right side against gravity to commands (M6). Speech is fluent. PEERL (4mm), right gaze preference noted. Left facial droop observed. Babinski sign absent. Patient is right hand dominant.GI: Abdomen soft, nontender, and nondistended with positive bowel sounds. GU: DeferredMusculoskeletal: Deferred Integumentary: Skin pale, cool and diaphoretic. No lower extremity edema.What data from Susan’s assessment and recent clinical history provided by Susan’s spouse is significant?Severe headachePossible LOCUrinary IncontinenceLeft sided weaknessWhat diagnosis do you suspect?Hemiplegic migraine Stroke Myocardial Infarction (MI) Cerebral Aneurysm Brain Tumor Cerebral Edema (CE)Drug Use InfectionSeizure(Smith & Massaro, 2015)Tests ordered by the physician. Rationale/Purpose/SignificanceCT or MRI: HeadCheck for edema, hemorrhage, clot, lesion or mass. In patients younger than 55 years presenting with stroke-like symptoms, MRI yields a lower rate of misdiagnosis than non-contrast CT because of a lower prevalence of vascular risk factors and a higher prevalence of central nervous system stroke mimics in this age group. However, non-contrast CT is the imaging test of choice for persons with suspected subarachnoid hemorrhage (SAH) (Newman-Toker et al, 2014).Chemistry PanelScreen for hypoglycemia, electrolyte imbalanceCBCScreen for anemia, bleeding disorders, thrombocytopenia and infectionUrine Toxicology ScreenScreen for presence of any prescription or illicit drugs (Esse et al, 2011) (Inal et al, 2104)Coagulation ProfileCheck clotting factors and bleeding disordersChest X-rayScreen for any gross abnormalities of heart and/or lungsEKGScreen for possible MI or other cardiac eventAnticipate ED Orders Clinical Significance/RationaleNPOIn the event that a procedure or surgical intervention is necessary. Pt. positive for nauseaStrict BedrestIncrease risk of fall due to decreased level of consciousness and left sided weakness.Neuro check q 15 minEvaluate for changes in current impaired neurological status.Diagnostic Tests, Results and RationalTestResultsRationaleUrine Toxicology ScreenNegative for ETOH, amphetamines, barbiturates, benzodiazepines, cocaine, heroin, Phencyclidine (PCP), and Tetrahydrocannabinol (THC).Screen for possible drug use including prescription and illicit drugs. None DetectedPT/PTTPT: 14.5 sec PTT: 27 secINR: 1.1Evaluate for bleeding and clotting disordersAll WNLCBC W/Diff & PLTWBC 5.2 K/mclRBC 4.66 M/mclHgb 14.1 g/dlHCT 42.7 %MCV 91.6 flMCH 30.3 pgMCHC 33.0 g/dlRDW 12.7 %Neutrophil (Neut) 50 % Lymphocyte (Lymph) 36 % Monocyte (Mono) 8 % Eosinophil (Eos) 5 % Basophil (Baso) 1 % Neut, Absolute 3.5 K/mcL Lymph, Absolute 2.5 K/mcL Mono, Absolute 0.6 K/mcL Eosl, Absolute 0.4 K/mcL Baso, Absolute 0.1 K/mcL Platelets 329 K/mclScreen for anemia, bleeding disorders, thrombocytopenia and infection. All WNLChemistryScreen for possible hypoglycemia or electrolyte imbalancesBUN14 mg/dLCreatine0.93 mg/dLNa145 mmol/LK5.0 mmol/LCl103 mmol/LCa10.0 mg/dLGlucose83 mg/dLNon-fasting glucose is WNLAlbumin4.9 g/dLBilibrubin (total)0.5 mg/dLProtein (total)7.1 g/dlALT27 U/LAST26 U/LALP91 U/LeGFR non-AA70 mL/min/1.73m2eGFR-AA81 mL/min/1.73m2CT: emergency, w/o contrastCT demonstrated acute hemorrhage in right frontal lobe, associated with vasogenic edema, and right-to-left midline shift. Presence of sulcal effacement suggests diffuse cerebral edema. CT scan results indicate acute intracerebral hemorrhage with diffuse cerebral edema.Family EducationWhat education is essential to communicate to Susan’s friends & family right now?Family and friends should be made aware of the additional diagnostic procedures that may be necessary, the course of treatment, and possible adverse effects of this diagnosis:Repeat CT, a CTA or MRITransfer to Neuro ICU for closer monitoring of ICP and vital signs Changes in mental status and physical status may occurPossible sedation and/or intubationCourse of treatment options (e.g. surgery)Possible need for PT and post-discharge continued care.Case Study ContinuedRationale/Purpose/SignificanceSoon after the CT, Susan became more lethargic with episodes of bradycardia to the 30s, without concomitant hypertension. She was subsequently intubated and given propofol and rocuronium. In addition, 50 grams of mannitol was administered IV. Once intubated, the Propofol infusion was titrated to maintain deep sedation. She was then moved to the neurological intensive care unit (NICU).Patient was intubated to preserve her airway with declining vital signs. The presence of increased ICP can cause bradypnea. Part of Cushing’s triad.Propofol and rocuronium administered routinely for sedation and initiation of mechanical ventilation Mannitol was administered to decrease ICP by reducing cerebral parenchymal cell water, total effect takes 20-30min. Mannitol also decreases blood viscosity (Witherspoon & Ashby, 2017).Propofol titration is administered to maintain moderate sedation (sleepy but awakens when spoken to or touched). Sedation with various sedative-hypnotics can reduce the metabolic requirements of the brain and thereby reduce cerebral blood volume (Oddo et al, 2016).Neuro ICU orders written. Rationale/Purpose/SignificancePosition in semi-fowlers HOB at 30-45 degrees, decreases risk of ventilator-associated pneumonia (VAP), and increases venous drainage (Mir, 2015).VS q 15minAssess for changes (deterioration or agitation)Finger stick glucose q 6hrPropofol sedation can cause insulin resistance(Yasuda, 2012).Strict I&OEvidence indicates that fluid management in brain-injured patients should generally be targeted at euvolemia using isotonic fluids (Van der Jagt, 2017)Neuro checks q 15minMaintain current level of sedationTests ordered by the physicianRationale/Purpose/SignificanceBlood gasesMonitor blood oxygenation levels. A decrease in blood oxygen levels, hypoxemia (<60 mmHg) indicates a need to administer oxygen (Colduvell, 2017).Repeat CT or CTARepeat CT or do CTA for additional diagnostics. CTA includes angiography to examine blood vessels (Maas et al, 2013).Case Study ContinuedRationale/Purpose/SignificanceOver a period of hours, while in the Neuro ICU, the patient’s GCS declined from 15 to 8. Given Susan’s deteriorating neurological status, a parenchymal fiber optic bolt was placed. Her initial ICP was 30 mmHg. She received an IV bolus of 50 grams of mannitol and 500 mL of 3% saline. Thereafter, 250 mL of IV 3% saline was administered every 6 hours. A radial arterial catheter was placed to maintain a cerebral perfusion pressure (CPP) between 60 and 80 mmHg with norepinephrine IV drip titration. Sedation with propofol and fentanyl was discontinued. IV phenytoin was initiated: loading dose of 700mg, then maintained with 100 mg IV infusion every 8 hours. Continuous electroencephalogram (EEG) monitoring was started and angiogram was ordered.A parenchymal fiber optic bolt was placed to monitor ICP as indicated by GCS decline. This tool has a lower complication rate, lower infection rate, and no chance of catheter occlusion or leakage (Raboel et al, 2012).IV Mannitol bolus administered to decrease ICP- initial reading was 30 mmHg. Normal ICP is 5-15 mmHgHypertonic saline is administered with mannitol when significant cerebral edema or increased ICP is suspected. Hyponatremia can increase Cerebral Edema, hypernatremia can lower ICP (Berger-Pelleiter et al, 2016).Arterial line place to maintain CPP at normal (60-100 mmHg). CPP= Mean arterial pressure (MAP) – ICPPhenytoin per drug protocol. Based on 18mg/kg loading dose then maintenance dose of 3-5mg/kg/d (GGC Medicines, 2018).EEG monitoring for possible seizure activity.Sedation with propofol and fentanyl was discontinued to better assess neurological status.Neuro ICU orders written. Rationale/Purpose/SignificanceNeuro checks q 15minMonitor for neurological decline. Depressed level of consciousness: confusion, restlessness, obtundation, progressive unresponsiveness. Abnormal cranial nerves findings (e.g. pupillary reaction), fixed and non-reactive to light. VS q 15minMonitor for changes in BP, R and P(Cushing’s triad).Monitor ICPIncreased ICP can indicate an increase in tissue volume, cerebral blood volume, or cerebrospinal fluid (CSF) volume.Monitor CPP. Call MD if CPP is outside of normal range.Maintain CPP at 60-80 mmHg, (normal 60-100 mmHg). CPP= Mean arterial pressure (MAP) – ICP Monitor EEG for abnormal activityAbnormal activity on EEG can indicate seizuresIV phenytoin loading dose of 700mg, then 100 mg IV infusion q 8 hr.Phenytoin per drug protocol to prevent seizures. Based on 18mg/kg loading dose then maintenance dose of 3-5mg/kg/d. (GGC Medicines, 2018)Tests ordered by the physicianRationale/Purpose/SignificanceBlood GasesMonitor blood oxygenation levels (Colduvell, 2017).CBC, Chem panelMonitor for changes in blood chemistries, and WBC count (infection).Case Study ContinuedRationale/Purpose/SignificanceOver the subsequent 24 hours, Susan’s ICP climbed up to 40 mmHg, despite multiple boluses of 3% saline and mannitol, heavy sedation, paralysis and targeted temperature management (TTM). Due to refractory ICP elevation, the patient underwent an emergent right fronto-temporo-parietal decompressive craniectomy without removal of the hematoma or AVM. The ICP after the decompressive hemicraniectomy was less than 20 mmHg. She was returned to the NICU. On postoperative day 0 and post-bleed day 1, Susan followed simple commands by showing 2 fingers on the right side.ICP up to 40 mmHg. Normal ICP is 5-15 mmHg.Multiple boluses of 3% saline and mannitol without reduction of ICPTTM has been shown to be effective in reducing ICP (Koyfman et al, 2017).Decompressive craniectomy is a neurosurgical procedure in which part of the skull is removed to allow a swelling brain room to expand without being squeezed (Komotar et al, 2011).NICU orders written. Why?Rationale/Purpose/SignificanceContinuous monitoring of VS including internal temp probe, during active cutaneous cooling.Patients may experience arrhythmias (bradycardia) associated with hypothermia. Target goal with TTM is: 35 degrees C (95F) – 34 degrees C (93.2F). Internal temperature probe is necessary for accurate core temp readings (Koyfman et al, 2017).Neuro checks q 15 min Monitor for neurological declineMeperidine 25 mg q3-4h PRN for shivering.Shivering will increase body temperature. Meperidine is the drug of choice and provides the greatest reduction in the shivering threshold. However, repeated dosing may result in accumulation of its primary metabolite, normeperidine, which can lower seizure threshold (Choi et al, 2011).Monitor ICPContinue other medical therapies that support treatment of increased ICP.Monitor and maintain CCPOften BP remains elevated during hypothermia as a result of peripheral vasoconstriction. Famotidine 20 mg IV bidHistamine H2-blockers (H2B) and proton pump inhibitors (PPI) are used commonly to prevent gastrointestinal bleeding in acute stroke, they are also implicated in the increased risk of pneumonia. (Arai et al, 2017)Case Study ContinuedRationale/Purpose/SignificanceOn post-op day 7 Susan was transferred to the floor where she has been assigned to you. She is awake, alert, and oriented to person, place and date. She has fluent speech with a mild dysarthria and left facial droop. Sensation is intact and motor strength is intact except for persistent right sided weakness. VS are WNLGCS is 15Continued right sided weaknessDay 7 post-op decompressive craniectomyWhat orders do you expect?Rationale/Purpose/SignificanceSequential compression devices Continuous use for deep vein thrombosis (DVT) prophylaxisEnoxaparin 40 mg SC once per dayLow-molecular-weight heparin can be used for DVT prophylaxisAcetaminophen ii tab q 4-6hr prnPain managementAssisted ambulationPt continues to have right sided weakness and is at high risk of fall.Neuro checks q 6hrPatient has stabilized, and neuro checks are not needed as frequently. Change in neuro status can indicate infection, stroke, edema, VS q shiftPatient has stabilized, and VS are not required as often. Increased temperature may indicate presence of infection.CBC and Chem panel q dayMonitor for changes in blood chemistries, and WBC count (infection).Post Discharge CarePatient’s current status at discharge: Right upper and lower limb strength are had been on admission.Susan has not regained pre-event strength back. Ambulates with assistance.Able to grasp items and feed herself. Susan’s sensation intact to light touch. Susan passed a swallow evaluation and was started on a mechanical soft diet. The patient will continue to participate with physical and occupational therapy. On post-op day 15, Susan was discharged to an acute rehabilitation center (ARC). VS- WNLNeuro- Fully oriented, senses have returned to pre-admission levels and lower limb strength has returned to normal Diet/Nutrition-She has been evaluated for swallowing and started a mech soft dietPT/OT- She is being referred to an ARC for additional therapy.Social- Patient’s spouse has been very supportive, involved in the treatment decisions, as well as with patient care (ADLs) and assisting with rehabilitation (PT and OT). Test your knowledge!QuestionsHow is hemorrhagic stroke different from ischemic stroke?What is the greatest risk factor associated with a stroke?What threat does blood from an ICH pose on the brain?What is Cushing’s triad?What surgical interventions are available to evacuate an ICH?How is ICP monitored and recorded?How is CPP calculated?Explain the difference between craniotomy and craniectomy.What are possible complications associated with a decompressive craniectomy?Will this patient need any additional surgical procedures related to this recent occurrence?What would be the long term prognosis for a patient that has experienced this scenario? AnswersHemorrhagic strokes occur less often (8-13%) than do ischemic strokes (87%) but have higher rates of mortality (40-50%). Hemorrhagic strokes are caused by the rupture of a weakened blood vessel, whereas ischemic strokes are caused by an obstruction in a blood vessel.HypertensionThe leaking blood puts too much pressure on brain cells and causes damage. It is seen when increased ICP decreases the cerebral blood flow significantly. A response is triggered that increases arterial pressure in order to overcome the increased ICP. The signs of Cushing’s triad are: hypertension and a widening pulse pressure (the difference between the systolic and diastolic BP), bradycardia, and bradypnea.Surgical intervention and treatment (external ventricular drain placement, hematoma evacuation, and decompressive hemicraniectomy) is often necessary for monitoring and prevention of secondary neurologic injury as a result of intracranial hypertension, herniation syndromes and brainstem compression. (Hemphill et al, 2015)Cerebral blood flow (CBF) is tightly linked to cerebral perfusion pressure (CPP), which is governed by both mean arterial pressure (MAP) and ICP through the following relationship, CPP = MAP-ICP. Accordingly, as ICP increases, MAP is increased, primarily through a rise in cardiac output, in order to maintain a steady CPP. In the presence of elevated ICP beyond the ability for compensation through elevation of MAP, CPP will be compromised and cerebral ischemia may follow. Some changes in mean ICP are expected under regular physiologic conditions, including changes in posture, brain activity, cardiovascular function, respiratory function and adrenergic tone. Alterations in ICP reach clinical significance when they are sustained longer than at least 5 min. Physiologic boundaries of mean ICP are 5–15 mm Hg in supine adults (Harary et al, 2018).CPP is the pressure required to move sufficient amounts of blood to the brain (cerebral blood flow), which maintains life and prevents brain ischemia. CPP=MAP – ICP ( MAP= SBP + 2(DBP) /3) (normal is 60 – 100mmHg) Craniotomy defines a procedure where the cranial cavity is accessed through removal of bone to perform a varietyof brain surgeries. Once the surgery is completed, the bone flap is returned to its previous position.Craniectomy differs from craniotomy in that the bone is not replaced to its previous position; instead it is stored forfuture insertion or may be discarded (depending on pathology – e.g. infection). This results in a cranial defectBleeding, infection, seizures, abnormalities in cerebrospinal fluid (CSF) absorption, further damage to the brain, stroke and/ or death. Stroke in the post-operative period may be the result of cardiogenic thromboembolism, distal embolism of foreign material (glue or embolizing material from endovascular procedures), systemic hypotension in the setting of vascular stenosis or occlusion, and artery-to-artery embolism as a result of catheter manipulation. Vascular occlusion may also result from cerebral edema, if brain herniation develops. (Kurland et al, 2015)Cranioplasty is an in evitable operation conducted after decompressive craniectomy(DC). During the DC a portion of the skull is removed and preserved for later use (cranioplasty). The primary goals of cranioplasty after DC are to protect the brain, achieve a natural appearance and prevent sinking skin flap syndrome (or syndrome of the trephined). (Cho et al, 2017)Unfortunately, it is not good and there is little research related to outcomes. ICH is a common subtype of stroke with a poor prognosis, high mortality and long-term morbidity. Of every 10 survivors of acute phase ICH at a young age, one died within 10 years after onset, male sex and diabetes being associated with increased mortality. Half the survivors did not achieve a favorable functional outcome, which was predicted by increasing age, initial stroke severity and intraventricular hemorrhage (Koivunena et al, 2015) (Tatlisumak et al, 2018).Reference ListArai, N., Nakamizo, T., Ihara, H., Koide, T., Nakamura, A., Tabuse, M., & Miyazaki, H. (2017). Histamine H2-Blocker and Proton Pump Inhibitor Use and the Risk of Pneumonia in Acute Stroke: A Retrospective Analysis on Susceptible Patients. PLoS ONE, 12(1), e0169300. , E., ?mond, M., Lauzier, F., Shields, J., & Turgeon, A. (2016). Hypertonic saline in severe traumatic brain injury: A systematic review and meta-analysis of randomized controlled trials. Canadian Journal of Emergency Medicine, 18(2), 112-120. doi:10.1017/cem.2016.12Cho, Y. J., & Kang, S. H. (2017). 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