Showing posts with label death. Show all posts
Showing posts with label death. Show all posts

Wednesday, September 25, 2013

Asthma Sucks... aka near death experience for my dh

What a week (actually, last week… I started writing this a week ago). It started off with an early morning trip to Target to take Jay to work by 4:30a.m.  Not three hours later and Jay almost left this bodily domain.


About 7:15, the phone rings, waking me from my nap between dropping Jay off at work and picking him up from work.  It was Jay’s job coach, L. He said that Jay was having an asthma attack. I quickly found out that it was a major attack, and the ambulance was on its way to get him. So I told him to tell the ambulance to take him to the university hospital (WAS the one hospital that he’d never stayed in, also the closest one to his work), and that I was on my way. In the ER, I met L. for the first time, and he explained everything that he knew about the asthma attack while we waited to be let back to the back.  Jay had been working for about 2 hours when his chest started to feel tight.  He decided to take his break and headed to the break room and used his puffer.  The puffer wasn’t really working for him.  That’s where L. found him and offered to take him home.  They started out of the building, and Jay’s breathing got worse and worse.  By the time L. pulled his car around to the front door, Jay was bent over and couldn’t speak.  He held up 9-1-1 with his fingers.  L. went in and told the manager, who called the ambulance while L. went back out to Jay. 


Once in the ER, they tried the bi-pap machine on him.  It wasn’t working, so after awhile, the ER doc told me they wanted to intubate him.  I agreed to it.  So L. and I had to leave the room while they did that.  I called his parents at that time to let them know what was happening, since it was so bad at that point.  I also called the A/C guy that was supposed to come out to the house that day (great timing, eh?).  He was fine with working in the house without me there; said they did it often.  I’d had the forethought to leave a key under the downspout catch.  So I told him where the key was and that I would check in on them periodically.


From then on, Jay was sedated until the next morning before they took the tube out (extubated him).  After he was intubated, they moved him up to the ICU.  L. left once they had him up there, and I promised to keep him updated on Jay’s status.  Once Jay was in the ICU, they wanted to put a central line in him.  I agreed to it, knowing that he’d had one before.  Meanwhile, I’m waiting and waiting to be let back into the room to see him.  They’d kicked me out right after they brought him up.  Then they had  a problem getting the central line in because his veins were partially occluded (probably from past scar tissue from past central lines), so they wanted to put a pic line in.  I agreed to that (again, he’s had one before).  So finally after all of that, hours later, I was able to go into his room and start answering the usual questions from the nurse (meds, medical history, etc.).  She felt bad that I had had to wait for so long (and hadn’t gotten to go eat any lunch), and gave me a complimentary card for $ 7 credit in the hospital cafeteria.  I didn’t use it until the next day. 


By around 3:00 or so, I decided to head back to the house and check on the A/C guys and eat something.  Jay was sedated and breathing better, so I knew nothing was going to change any time soon.  I’d already spoken to Jay’s parents and his sister several times during the day.  I knew Jay’s dad was trying to find someone to drive down with him, but hadn’t found anyone yet.  At home, everything was going fine with the A/C replacement, so I hung out until they finished.  On the way back, I picked up a friend to sit with me and sent a text to his sister that I was heading back to the hospital.  She texted back that they were on their way there, had just gotten off the interstate. So I quickly texted back to park by the Patient Discharge area and take the elevators up from there.  They stayed for a few hours.  I know it really bothered his sister to see Jay intubated, and then she saw that they had his arms strapped down to the bed.  I explained it was so that if he woke up, he wouldn’t try pulling the tubes out of his mouth.  Jay’s dad just took it all in stride.  He worked as a medic in the military back in the day, so he’s seen worse. 


Tuesday morning, I got back to the hospital in time for visiting hours to start at 8am.  They had taken Jay off the sedative, and he was starting to come around.  His breathing was much better, and they talked about extubating him that morning.  By mid-morning they did.  He doesn’t remember anything from that morning though.  I would later have to repeat almost everything I had told him that morning:  how he’d gotten to the hospital, my calling his work, the A/C guys, his sister & dad coming the day before… Later that day, they took out the catheter from his penis.  My friend and her husband came by to visit before going to their childbirth class.  By then, the hospital had gotten back the MRSA results on Jay, and he had tested positive again, so visitors had to suit up in “protective gear”.  Such a weird practice at the hospital.  We were told that he would probably move out of ICU that day.  Of course, it didn’t happen.  There had been some concern about his kidney because his creatinine level had gone up from the day before.  It had been 1.7 when he was in the ER Monday morning, but was 2.1 in the ICU Tuesday morning.  The nephrologist was pretty sure it was because of all the drugs and stuff they’d put through him in the past 24 hours, but they wanted to be sure. So they pushed a lot of fluids.


Wednesday morning, his creatinine was back down to 1.7, and they moved him to a regular room.  He spent 24 hours in there, and got to go home on Thursday.  We already had an appointment with the nephrologist for Friday, so we just set up an appointment with his primary for follow up on his breathing.  On Friday, the nephrologist was quite surprised that Jay had gotten out of the hospital so quickly.  He was able to look at his x-rays and whatnot from the hospital.  He said that usually an asthma attack that bad has people staying in the hospital for a couple of weeks.  Even better, his creatinine on the last day in the hospital was at 1.3. 


This asthma attack was the worst one that Jay has ever had.  And I have said many times over the past few years, that it’s not the diabetes that’s going to kill him, it’s the asthma.  It almost did.  Jay has said several times since that day, that he thought for sure he was not going to make it; that he was going to die.  He said he prayed and prayed to God, while standing, bent over, outside Target, to not let him go this way, to keep him alive.  And He did.


Tuesday, September 17, 2013

death after hospital overdose treatment ...How ? Dehydration and/or insulin induced HYPOglycemia and/or HYPOvolemia ??


“Every Day And In Every Way I Am Getting Better And Better“…
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Published Date: 19 June 2008



A MOTHER died at her home from medical complications a day after BEING TREATED FOR taking an overdose.



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 …



“She was staggering and was slurring her words,” he said.


“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


[ON WHAT DATE ?].

“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.







The full article contains 381 words and appears in Evening Leader Chester newspaper …






  • 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.






Contents










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




Main article: Extracellular 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



  1. ^ 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.

  2. ^ Danic B, Gouezec H, Bigant E, Thomas T (2005). “Incidents of blood donation”. Transfus Clin biol Jun;12(2):153-9. PMID 15894504

  3. ^ [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


  4. ^ M.J. McKinley and A.K. Johnson (2004). “The Physiological Regulation of Thirst and Fluid Intake“. News in Physiological Sciences 19 (1): 1-6.




See also





External links