Daisy Little Simpson's Death

Daisy Little died tragically at age 32 on February 20th, 1936. She left behind her husband and six children ranging in age from 2 months to 12 years. Little is known about the circumstances surrounding her untimely death. Family discussions include that she may have died from complications arising from the birth of her youngest child, Andrew Lewis or that she died from malnutrition as it is thought that her husband Shirley did not provide for her or his family. It is known that upon her death, Shirley gave up his children dispersing them among Daisy's sisters.

Reviewing Daisy's Death certificate, it appears that she died of pneumonia and the complications of a stroke which was likely the result of chronic hypertension (high blood pressure) and childbirth.

The Death Certificate indicates that she was admitted to Hillman Hospital on February 11, 1936 paralyzed on the right side of her body and that she suffered from high blood pressure. The primary causes of death shown are Bronchopneumonia and hemiplegia (paralysis on one side of the body commonly resulting from a stoke). It is likely that the combination of her high blood pressure and her recent childbirth led to a stroke as evidenced by her paralysis. She then likely contracted pneumonia while in the hospital and died.

The current average age of individuals suffering a stroke in the United States is 70. So, it is rare that Daisy had a stroke at the age of 32. Additionally, the incidence of stroke brought on by pregnancy or childbirth is 8 in 100,000, also very rare. However, according to blackhealth.com, the risk of stroke during the six weeks after childbirth is 9 to 28 times higher than that for non-pregnant or post-partum women. Daisy gave birth 7 weeks before her apparent stroke.

Daisy's Death Certificate is summarized below:		Daisy Little Simpson Death Certificate
Personal & Statistical Data Place of Death: Jefferson County, Birmingham, AL, Hillman Hospital Place of Residence: 5220 Division Ave., East Lake Full Name: Mrs. Daisy Simpson Sex: Female Race: White Marital: Married Husband: Mr. Shirley Simpson Date of Birth: Apr 9, 1903 Age: 32 years, 10 months, 11 days Occupation: Housework Birthplace: St. Clair County, AL Father: ? Little Mother: Doschia McLaughlin born Jefferson County, AL Informant: Mr. Shirley Simpson, 5220 Division Ave., East Lake Burial: Leeds, 2-20-36 Undertaker: N. B. Whitmire Filed: 2-20-36 by J. F. Newsome	Medical Certificate of Death Date of Death: 2-20-36 Dr. attended deceased from 2-11 to 2-20 1936 Time of Death 5:09 AM Principle Causes of Death and date of onset: Bronchopneumonia on 2-18-36 and Hemiplegia on 2-11-36 Contributory Conditions: Hypertensive Cardiovascular Disease Was disease related to occupation: No Signed: F. H. Parsler, M.D.

Detailed Medical Explanation
Stroke
A stroke occurs when the blood supply to part of the brain is suddenly blocked or when a blood vessel in the brain bursts, spilling blood into the spaces surrounding brain cells. In the same way that a person suffering a loss of blood flow to the heart is said to be having a heart attack, a person with a loss of blood flow to the brain or sudden bleeding in the brain can be said to be having a "brain attack."

Paralysis is a common feature of stroke, often on one side of the body (hemiplegia). The paralysis or weakness may affect only the face, an arm, or a leg or may affect one entire side of the body and face.

A person who suffers a stroke in the left hemisphere of the brain will show right-sided paralysis or paresis. Conversely, a person with a stroke in the right hemisphere of the brain will show deficits on the left side of the body.

Stroke and Childbirth
[] studies have demonstrated that pregnancy and childbirth can put a woman at an increased risk for stroke. Pregnancy increases the risk of stroke as much as three to 13 times. Of course, the risk of stroke in young women of childbearing years is very small to begin with, so a moderate increase in risk during pregnancy is still a relatively small risk. Pregnancy and childbirth cause strokes in approximately eight in 100,000 women. Unfortunately, 25 percent of strokes during pregnancy end in death, and hemorrhagic strokes, although rare, are still the leading cause of maternal death in the United States. Subarachnoid hemorrhage, in particular, causes one to five maternal deaths per 10,000 pregnancies.

A study sponsored by the NINDS showed that the risk of stroke during pregnancy is greatest in the post-partum period – the 6 weeks following childbirth. The risk of ischemic stroke after pregnancy is about nine times higher and the risk of hemorrhagic stroke is more than 28 times higher for post-partum women than for women who are not pregnant or post-partum. The cause is unknown.

Hemiplegia
is a condition in which one-half of a patient's body is paralyzed. Hemiplegia is more severe than hemiparesis, wherein one half of the body is weakened but not paralysed. It can be congenital (occurring before, during, or soon after birth) or acquired (as from illness or stroke). It is usually the result of a stroke, although disease processes affecting the spinal cord and other diseases affecting the hemispheres are equally capable of producing this clinical state. Hemiplegia can be a more serious consequence of stroke than spasticity. Cerebral palsy can also affect one hemisphere, resulting in limited function. This does not cause paralysis but instead causes spasms. Cerebral palsy where this is the only symptom is often referred just as hemiplegia.
Other causes include Type 2 diabetes mellitus, which can lead to transient hemiplegia, a type of spinal injury called Brown-Sequard syndrome, and injections of local anaesthetic given intra-arterially rapidly, instead of given in a nerve branch. Lesions in the posterior limb of the internal capsule can also lead to hemiplegia.

Hypertensive Cardiovascular Disease or HCVD
[High] blood pressure (BP) can lead to a variety of changes in the myocardial structure, coronary vasculature, and conduction system of the heart. These changes can lead to the development of left ventricular hypertrophy (LVH), coronary artery disease, various conduction system diseases, and systolic and diastolic dysfunction of the myocardium, which manifest clinically as angina or myocardial infarction, cardiac arrhythmias (especially atrial fibrillation), and congestive heart failure (CHF).

Thus, hypertensive heart disease is a term applied generally to heart diseases, such as LVH, coronary artery disease, cardiac arrhythmias, and CHF, caused by direct or indirect effects of elevated BP.

[Cardiac arrhythmias,one of] the [] various cardiac effects of hypertension [] is described [below]:

Cardiac arrhythmias commonly observed in patients with hypertension include atrial fibrillation, premature ventricular contractions, and ventricular tachycardia. The risk of sudden cardiac death is increased. Various mechanisms thought to play a part in [] arrhythmias include altered cellular structure and metabolism, inhomogeneity of the myocardium, poor perfusion, myocardial fibrosis, and fluctuation in afterload. All of these may lead to an increased risk of ventricular tachyarrhythmias.

Atrial fibrillation (paroxysmal, chronic recurrent, or chronic persistent) is observed frequently in patients with hypertension. In fact, elevated BP is the most common cause of atrial fibrillation in the Western hemisphere. In one study, nearly 50% of patients with atrial fibrillation had hypertension. Although the exact etiology is not known, left atrial structural abnormalities, associated coronary artery disease, and LVH have been suggested as possible contributing factors. The development of atrial fibrillation can cause decompensation of systolic and, more importantly, diastolic dysfunction, owing to loss of atrial kick, and it also increases the risk of thromboembolic complications, most notably stroke.

Cerebral involvement in hypertensive cardiovascular disease
Stroke and dementia in hypertension are the culmination of a complex and largely silent pathogenesis that involves atherosclerosis, vascular remodelling, white matter lesions (WMLs), lacunae and microaneurysms. WMLs in apparently asymptomatic hypertensive persons are associated with incipient cognitive impairment and cardiac hypertrophy. Longitudinal studies have established a link between WMLs and future stoke, and between cognitive decline and hypertension. A small, sustained lowering of systolic/diastolic blood pressure reduces the relative risk of stroke by about 35–40%. A favorable prognosis appears to be not simply a matter of blood pressure control. Angiotensin II receptor blockers are more effective than beta-blockers in reducing the risk for stroke, dementia and left ventricular hypertrophy in hypertensive persons, despite similar reductions in blood pressure. The mechanisms of cognitive decline in hypertension are unclear, but it is known that vascular remodelling and endothelial dysfunction in small arteries are better corrected by blockade of the renin-angiotensin-aldosterone system (RAAS) than by beta-blockade.