A 67-Year-Old Man With an Acute Neurological Event: Presentation, Diagnosis, and Prognosis
Ronald N. Rubin, MD1,2—Series Editor
1Lewis Katz School of Medicine at Temple University, Philadelphia, Pennsylvania
2Department of Medicine, Temple University Hospital, Philadelphia, Pennsylvania
Rubin RN. A 67-year-old man with an acute neurological event: presentation, diagnosis, and prognosis. Consultant. 2020;60(6):e10. doi:10.25270/con.2020.06.00002
The author reports no relevant financial relationships.
Ronald N. Rubin, MD, Temple University Hospital, 3401 N Broad St, Philadelphia, PA 19140 (email@example.com)
A 67-year-old man was brought to the emergency department for evaluation of an evolving neurological event. He had been watching evening TV with his wife as is usual for them when he reported having an acute headache and nausea. He got up to go into the bathroom in case of emesis and to obtain some analgesics, but shortly thereafter, his wife heard him fall. She called emergency medical services, and her reported immediate findings combined with those of the ambulance personnel revealed that he was significantly aphasic within minutes and had paralysis of his right arm and leg. Facial asymmetry was also noted. There were no seizures.
His medical history was positive for mild type 2 diabetes, which had been well-controlled (recent hemoglobin A1c level of 6.0%) with diet and metformin. He had had hypertension for many years, which was currently being treated with losartan, 100 mg/d, and a diuretic. There was no history of antecedent transient ischemic attack or other neurological event.
On physical examination, vital signs were as follows: blood pressure, 170/105 mm Hg; pulse rate, 66 beats/min; respiratory rate, 12 breaths/min; and temperature, 37 °C. Doll’s eye movement was present, and pupils were equal, round, and reactive to light and accommodation, without nystagmus. There were no carotid bruits. The lungs were clear, and the heart had regular rhythm without murmurs. There was bilateral 2+ ankle and pedal edema. Neurological examination showed a retained gag reflex. He was arousable but significantly obtunded with depressed mentation. There was flaccid paralysis of his right side.
Stat laboratory tests revealed a normal complete blood cell count. Results of a basic metabolic panel showed a glucose level of 136 mg/dL, normal electrolyte levels, and a creatinine clearance of 59 mL/min/1.73 m2. Troponin levels were within normal limits, and electrocardiography showed regular rhythm and no injury currents. Voltage criteria for left ventricular hypertrophy were present.
Answer: C, rapid CT scanning or MRI is the initial study and maneuver of choice.
The patient presented here serves as an example of the presentation, demographics, diagnosis, and prognosis of the devastating situation of cerebral intraparenchymal hemorrhage (IPH) from the general physician’s viewpoint. IPH initially fits into the diagnosis of “stroke” and accounts for roughly 20% of stroke cases, with the remainder due to the more common thromboembolic “ischemic” pathophysiology.1 Nonetheless, IPH continues to cause higher mortality and morbidity than all other forms of stroke, with a reported 1-year survival rate of 40% and 10-year survival of 24%, with recovery of functional independence in only 12% to 39% of cases—serious morbidity and mortality, indeed.1
A variety of pathophysiologic lesions cause IPH. By far, the most common is rupture of small arteries, usually perforating arteries deep in the brainstem—the lenticulostriate arteries.1 The 2 major underlying causes for such rupture are hypertension-induced degenerative changes, which is an old and very well-known causation, and the more recently described cerebral amyloid angiopathy (CAA), wherein β-amyloid deposition in small cortical arteries and arterioles weaken them and predispose to rupture.1
For now, the most significant risk factor for IPH by far is hypertension compared with normotensive controls.2 Other less common underlying etiologies include the presence of a congenital AVM, the presence of a hemorrhagic primary brain tumor or metastatic lesion, cerebral vasculitis associated with autoimmune diseases, and coagulopathy associated with the use of the ever-growing number of anticoagulant regimens.1 These are all far less common causes than hypertension and CAA, making Answer A an incorrect statement.
Regardless of underlying causation, the initial IPH is not the only event of concern, since rebleeding (usually within the first year) remains a significant concern in all IPH cases. For example, IPH due to hypertension has a 3.2% to 7.8% rebleeding risk,3 and CAA carries up to a 3.8% rebleeding risk.4 Answer B significantly understates these numbers and thus is also an incorrect statement.
Patients experiencing an IPH will present similarly to the presentation of the general and age-old stroke syndrome of acute focal neurological deficit, headache, or seizure, either alone or in any combination. Similarly, any and all combinations of upper- and/or lower-extremity paralysis and dysphasia/aphasia will be present in most cases, and one cannot differentiate IPH from ischemic stroke based on these signs and symptoms. However, clues to IPH do include the presence of depressed mentation and headache, which are both less common features of ischemic strokes; this makes Answer D yet another incorrect statement.
The clues to an increased likelihood of a secondary causation of IPH include an age younger than 65 years, nonsmoker status, the presence of intraventricular hemorrhage on imaging results, and of course, no history of hypertension.1,3
Prompt and accurate diagnosis (particularly, differentiating IPH from ischemic causation) is mandatory on at least two counts. First, the acute therapeutics (which will be reviewed and discussed in a subsequent “What’s the ‘Take Home’?” column) are very different, with aggressive blood pressure control and surgical decompression in play for the former, and a permissive degree of hypertension control, thrombolytics, and catheter-directed thrombectomy in play for the latter.5 And second, for any stroke, the window of efficacy is narrow, with 3 to 6 hours being a commonly used optimum time frame.5
For IPH specifically, 25% of patients demonstrate clinical deterioration in transport to the hospital, and a similar number deteriorate while in the emergency department.6 Therefore, rapid imaging, either CT scanning or MRI, needs be performed quickly. This imaging study will accomplish a variety of things: First, IPH vs thromboembolic stroke will be definitively determined. Second, the study can demonstrate high-risk characteristics for further deterioration, such as midline shift of 2 mm or more and/or the presence of associated intraventricular bleeding, which may indicate the need for early neurosurgery. And the initial study also will serve as a baseline for monitoring hematoma growth, which is yet another morbidity/mortality indicator, as well as another guide regarding the need for neurosurgical intervention or not.5,7 Thus, Answer C is the correct choice here.
More-detailed and specific management issues will be addressed and discussed in the next installment of “What’s the ‘Take Home’?”
The patient’s Glasgow Coma Scale score was 11. Urgent CT scans revealed the presence of a supratentorial IPH in the region of the thalamus measuring approximately 25 to 30 mL. There was no associated intraventricular hemorrhage and no findings typical of CAA. The patient was promptly placed in the neurological intensive care unit, with urgent consultation with neurology and neurosurgery specialists.
Cerebral IPH accounts for approximately 20% of stroke cases. IPH has a higher mortality and morbidity (disability) risk than the more common thrombotic stroke. Major predisposing pathophysiologic causes are hypertension and amyloid angiopathy, even in recent decades with availability of better antihypertensive agents. Secondary causes are less common but treatable and include AVMs, anticoagulation misadventures, vasculitis secondary to autoimmune disease, and primary/metastatic neoplasms. Clues to the presence of IPH vs thrombotic causation include history of hypertension, presence of seizure or headache, and depressed mentation. Imaging—either CT or MRI—is urgently indicated in suspected cases to confirm IPH (which is treated differently from thrombotic stroke) and to monitor/confirm findings (eg, hematoma size and growth, presence of intraventricular bleeding, extent of midline shift) that will influence management (eg, neurosurgical intervention) and prognosis.
- Gross BA, Jankowitz BT, Friedlander RM. Cerebral intraparenchymal hemorrhage: a review. JAMA. 2019;321(13):1295‐1303. doi:10.1001/jama.2019.2413
- O’Donnell MJ, Xavier D, Liu L, et al. Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study. Lancet. 2010;376(9735):112‐123. doi:10.1016/S0140-6736(10)60834-3
- Biffi A, Anderson CD, Battey TWK, et al. Association between blood pressure control and risk of recurrent intracerebral hemorrhage. JAMA. 2015;314(9):904‐912. doi:10.1001/jama.2015.10082
- O’Donnell HC, Rosand J, Knudsen KA, et al. Apolipoprotein E genotype and the risk of recurrent lobar intracerebral hemorrhage. N Engl J Med. 2000;342(4):240‐245. doi:10.1056/NEJM200001273420403
- Hemphill JC III, Greenberg SM, Anderson CS, et al; American Heart Association Stroke Council; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. 2015;46(7):2032‐2060. doi:10.1161/STR.0000000000000069
- Fan J-S, Huang H-H, Chen Y-C, et al. Emergency department neurologic deterioration in patients with spontaneous intracerebral hemorrhage: incidence, predictors, and prognostic significance. Acad Emerg Med. 2012;19(2):133‐138. doi:10.1111/j.1553-2712.2011.01285.x
- Hemphill JC III, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001;32(4):891‐897. doi:10.1161/01.str.32.4.891