“Every Day And In Every Way I Am Getting Better And Better“…
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Jayne Elizabeth Wildsmith died at the Countess of Chester Hospital on July 30 after suffering a pulmonary embolism and deep vein thrombosis.
TWICE ??
Cheshire coroner Nicholas Rheinberg heard Mrs Wildsmith, 45, of Denbigh Close, Ellesmere Port, had a long history of depression, suffered with asthma and diabetes and was obese.
Mr Rheinberg read a statement by Mrs Wildsmith’s GP, Dr Catherine Elizabeth Wall, who said the depression was exacerbated by a problem with alcohol.
Mrs Wildsmith told Dr Wall on July 9 she had stopped taking her medication and was feeling much better.
She returned to the doctor’s on July 27 saying she was feeling anxious and having suicidal thoughts [SSRI ? / STATINS ?].
On July 29 she was admitted to hospital after taking an overdose.
Sarah Jayne Edwards, of Derwent Court, Ellesmere Port, gave evidence at the Chester inquest and said her sister had been divorced since 1992.
Mrs Wildsmith’s son, Martin Edwards, said he was awoken by his mother on July 30. She told him she had taken an overdose and had called an ambulance.
Mr Edwards said his mother arrived home at 6.30pm [ON WHAT DATE ?] and had to be helped out of the taxi.
HYPOGLYCEMIA / DEHYDRATION SYMPTOMS …
“I couldn’t smell any alcohol and thought it was the result of the overdose.” He said he gave her some soup before taking her to bed and checked on her every 15 minutes. After the third check, she seemed fine and he went to bed himself. The next day he got up at noon and checked on his mother at 1.30pm “She was lying as I had left her. I tried to wake her and felt her hand and it was cold,” he said. Dr Sally Ann Hales, pathologist at Countess of Chester Hospital, said Mrs Wildsmith’s obesity and osteoarthritis were contributory factors in her death. The cause of death was given as pulmonary embolism arising partly as a result of immobility. Mr Rheinberg, who recorded a verdict of death by natural causes, said Mrs Wildsmith’s overdose was a “dramatic gesture” and not a serious attempt to take her own life.
[ON WHAT DATE ?].
- Last Updated: 19 June 2008 11:50 AM
- Source: Evening Leader Chester
- Location: Mold
HYPOvolemia …
In physiology and medicine, HYPOvolemia (also HYPOvolaemia) is a state of decreased blood volume; more specifically, decrease in volume of blood plasma.
Volumetric thirst can be caused by a number of things including bleeding and diarrhea. Volumetric thirst arises when the volume of blood plasma decreases.
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Causes
Common causes of HYPOvolemia can be dehydration,
bleeding, vomiting[1], severe burns and drugs such as diuretics or vasodilators typically used to treat hypertensive individuals. Rarely, it may occur as a result of a blood donation[2], sweating[1], and alcohol consumption[1].
Effects
Severe hypovolemia leads to hypovolemic shock.
A low blood volume can result in multiple organ failure, kidney damage and failure, brain damage, coma and death (desanguination).
Bodily response
To respond to hypovolemia is a task for the body fluid balance systems as well as osmotic balance systems.
Following an acute response, this function is accomplished by two sets of receptors; one in the kidneys and the other in the heart.
Acute response …
- Further information: Baroreflex
The first response to HYPOvolemia is an inversed baroreflex, where a lack of activation of baroreceptors results in elevation of total peripheral resistance and cardiac output via increased contractility of the heart, heart rate, and arterial vasoconstriction,[3]which tends to increase blood pressure.
Kidney
The kidneys have a specialized set of cells that enable the recognition of changes in blood flow to the kidneys.[1]
Naturally, these cells detect the presence of hypovolemia and react accordingly to the loss of blood volume.
These cells secrete a hormone called renin when there is a decrease in the flow of blood to the kidneys.[1]
Renin flows into the blood and there, initiates the conversion of a protein called angiotensinogen to angiotensin.[1]
In order to exert its effects on the body, angiotensin I must be converted by enzymes into its active form, angiotensin II.
Physiologically, angiotensin II stimulates the release of hormones by the posterior pituitary gland (ADH, also known as vasopressin) and the adrenal cortex (aldosterone).
Aldosterone causes the kidneys to reabsorb sodium, leading to the reabsorption of water. ADH (vasopressin) also causes the kidneys to reabsorb water.
Angiotensin II increases blood pressure by contracting arterial muscles.
Heart
- Further reading:Atrial natriuretic peptide
The next set of receptors responsible for detecting volumetric insufficiency are located in the heart atria. Commonly referred to as stretch receptors, these atrial baroreceptors detect the amount of blood that is being pumped back into the heart from the veins.[1] The body constantly returns blood to the heart through veins. Therefore, when the volume of blood being transported back to the heart is decreased, these receptors detect the change in the amount of blood thereby reducing the release of atrial natriuretic peptide.
Thirst
Both the activation of the renin angiotensin system and the decrease in atrial natriuretic peptide, along their other functions, contribute to elicit thirst, by affecting the subfornical organ.[4]
Other response …
Furthermore, as intravascular fluid decreases, blood pressure is reduced and the body attempts to compensate by moving fluid from other cellular compartments into the vasculature.
Fluid is transferred from all of the fluid compartments in the body, including intracellular, interstitial and other extravascular compartments.[1]
Diagnosis
Clinical symptoms may not present until 10-20% of total whole-blood volume is lost.
Hypovolemia can be recognized by elevated pulse, diminished blood pressure, and the absence of perfusion as assessed by skin signs (skin turning pale) and/or capillary refill on forehead, lips and nail beds. The patient may feel dizzy, faint, nauseated, or very thirsty. These signs are also characteristic of most types of shock.
Note that in children, compensation can result in an artificially high blood pressure despite hypovolemia. This is another reason (aside from initial lower blood volume) that even the possibility of internal bleeding in children should always be treated aggressively.
Also look for obvious signs of external bleeding while remembering that people can bleed to death internally without any external blood loss.
Also consider possible mechanisms of injury (especially the steering wheel and/or use/non-use of seat belt in motor vehicle accidents) that may have caused internal bleeding such as ruptured or bruised internal organs. If trained to do so and the situation permits, conduct a secondary survey and check the chest and abdominal cavities for pain, deformity, guarding or swelling. (Injuries to the pelvis and bleeding into the thigh from the femoral artery can also be life-threatening.)
Treatment
Minor HYPOvolemia from a known cause that has been completely controlled (such as a blood donation from a healthy patient who is not anemic) may be countered with initial rest for up to half an hour.
Oral fluids including moderate sugars (apple juice is good) and rich in electrolytes are needed to replenish the organism of lost sodium ions.
Furthermore the advice is to the donor to eat good solid meals with proteins for the next few days.
Typically, this would involve a fluid volume of less than one liter (1000 ml), although this is highly dependent on body weight.
Larger people can tolerate slightly more blood loss than smaller people.
More serious HYPOvolemia should be assessed by a nurse or doctor. When in doubt, treat HYPOvolemia aggressively.
First Aid
External bleeding should be controlled by direct pressure. If direct pressure fails, other techniques such as elevation and pressure points should be considered. The tourniquet should be used in the case of massive hemorrhage i.e. arterial bleeds, such as the femoral artery, as a last resort, for the use of a tourniquet can easily kill all the tissue below its application upon a limb, making amputation necessary. If a first-aider recognizes internal bleeding, the life-saving measure to take is to immediately call for emergency assistance.
Field Care
Emergency oxygen should be immediately employed to increase the efficiency of the patient’s remaining blood supply. This intervention can be life-saving.
The use of intravenous fluids (IVs) may help compensate for lost fluid volume, but IV fluids cannot carry oxygen in the way that blood can. See also emergency medical services for a discussion of techniques used in IV fluid management of hypovolemia.
Hospital Treatment
If the HYPOvolemia was caused by medication, the administration of antidotes may be appropriate but should be carefully monitored to avoid shock or the emergence of other pre-existing conditions.
Blood transfusions coupled with surgical repair are the definitive treatment for hypovolemia caused by trauma. See also the discussion of shock and the importance of treating reversible shock while it can still be countered.
History
HYPOvolemia has historically been termed desanguination (from Latin sanguis, blood), meaning a massive loss of blood. The term was widely used by the Hippocrates in traditional medicine practiced in the Greco-Roman civilization and in Europe during the Middle Ages. The word was possibly used to describe the lack of personality (by death or by weakness) that often occurred once a person suffered hemorrhage or massive blood loss.
References
- ^ a b c d e f g h Carlson, N. R. (2005). Foundations of Physiological Psychology: Custom edition for SUNY Buffalo. Boston, MA: Pearson Custom Publishing.
- ^ Danic B, Gouezec H, Bigant E, Thomas T (2005). “Incidents of blood donation”. Transfus Clin biol Jun;12(2):153-9. PMID 15894504
- ^ [Influence of age on the cardiovascular response during graded haemorrhage in anaesthetized rats] Andrej Banic 1, Gisli H. Sigurdsson 2, Anthony M. Wheatley 3 1Department of Plastic Surgery, University of Berne, Inselspital, CH-3010 Bern, Switzerland
^ M.J. McKinley and A.K. Johnson (2004). “The Physiological Regulation of Thirst and Fluid Intake“. News in Physiological Sciences 19 (1): 1-6.
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