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mistydeyes · 1 year ago

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141 and what their patient file looks like

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summary: This is what I imagine everyone's favorite pharmacist as well as medics see when they look at 141's medical file.

Based on this pharmacist and 141 interactions

pairing: Task Force 141 x pharmacist!Reader

warnings: medical/pharmacy terminology, medical inaccuracies, swearing, depiction of wounds, mention of substance use disorder and abuse

Terms

PMH - Past medical history - the total sum of a patient's health status prior to the presenting problem

FH - Family history - contributing family history, generally parents and siblings

SH - Social history - contributing social behavior and routine

a/n: not canon at all! this is just a reference for me

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Price

PMH

Height: 1.88 m (6' 2'')

Weight: 93 kg (205 lbs)

Blood type: O+

Extensive physical injuries

21+ stab wounds - 2 required antibiotics for recurrent infection

9x bullet wound - 5x in the extremities, 4x in the chest (no perforation of vital organs), healed without complication

5x abrasion collar - 1 near right eyebrow became infected following medical eval and stitches

3x diagnosed concussion

Aspirin-sensitivity

Previously evaluated for tinnitus and hearing loss

Father - deceased at 76 from liver disease - 50 pack years, mycardial infarction (x2)

Mother - deceased at 84 due to chronic heart failure (CHF) -Glaucoma, asthma, CHF

Sister - Sports induced asthma, hypothyroidism

Negative family history of diabetes, hypertension, and cancer

Smokes - 30 pack years

Drinks regularly - 4-5 hard liquor each weekend; 1 glass of whiskey occasionally

Physically active - Enjoys recreational activities such as hiking, swimming, and biking

Has 1 dog, currently under the care of pt's younger sister

History of monogynous long term relationships, currently single

Medication list + indications

Amoxicillin/Clavulanic acid 625mg - Infection

Morphine 15mg + Ketamine 3mg - IV - Pain

Paracetamol 750mg - Pain

Buproprion SR 150mg - Smoking cessation - not-taking est 2004

Allergies

Aspirin allergy - Reaction: hives and asthma - ONLY PRESCRIBE PARACETAMOL

No environmental, food, or animal allergies

Notes

Patient has denied smoking cessation options

Soap

PMH

Height: 1.88 m (6' 2'')

Weight: 91 kg (200 lbs)

Blood type: O+

7x stab wound - 6 required antibiotics for recurrent infection, 2 MRSA resistant

2x bullet wound - 2x in lower extremities, healed with no complication

6x abrasion collar

2x broken collar bone - healed, with no complication

Lactose sensitivity - Recurrent IBS if ingested

Chipped first left molar following opening a beer with teeth

Father deceased at 68 due to heart failure - Type 2 Diabetes Mellitus, high cholesterol

Mother - Stage I HTN (hypertension)

Sister #1 - Postpartum depression, generalized anxiety disorder

Sister #2 - Elevated cholesterol/triglycerides

Brother - No known chronic health issues

Positive family history of diabetes and hypertension, but no cancer

Drinks regularly and heavily - 8-12 beers and 2-3 glasses of hard liquor each weekend; 1 glass of scotch occasionally

Smokes socially - 5 pack years

Physically active

Close relationship with family, has 4 dogs at home under the care of pt's mothers

Avid fan of The Glasgow Football Club

Medication list + indications

Clindamycin 300mg with ciprofloxacin 400mg - Infection

Amoxicillin/Clauvanic acid 625mg - Infection

Vancomycin 18mg/kg - MRSA resistant infection

Paracetamol 500mg - Pain

Morphine 15mg IV - Pain

Doxycycline 100mg - Acne discontinued in 2004

Allergies

Insect stings - Observed anaphylaxis to childhood bee sting

Notes

Patient demonstrates medication non-adherence, counsel ESPECIALLY with antibiotics

Scored 6 on Alcohol use disorders identification test for consumption (AUDIT C)

Gaz

PMH

Height: 1.86 m (6' 1'')

Weight: 93 kg (205 lbs)

Blood type: B-

3x stab wound - healed, no complications

1x broken collar bone

2x broken femur

Diagnosed concussion - evaluated in Oct. '19

Father - Type 1 Diabetes, high cholesterol

Mother - Vitiligo, Stage 3 breast cancer

Positive family history of maternal cancer and diabetes, but no hypertension

Social drinker - 3-4 beers each weekend

Does not smoke

Physically active - Enjoys morning and evening runs

Enjoys spicy food and tries to introduce into diet

When on leave, enjoys attending concerts and music festivals

Medication list + indications

Piriteze 10mg - Allergic rhinitis

Fluticasone Propionate - 93 mcg/actuation - Allergic rhinitis

Paracetamol 500mg - Pain

Allergies

Seasonal - Pollen and pet dander

β-Lactam allergy - Reaction: anaphylaxis evaluated in '19

Notes

Organ donor

Ghost

PMH

Height: Weight: 1.93 m (6' 4'')

WeighT: 100 kg (220 lbs)

Blood type: AB-

Extensive cuts and scarring to entire body

4+ stab wounds - healed, no complications

Gun shot to lower abdomen - healed, no complications, evaluated in Nov. '22

13+ collar abrasion

2x broken nose

Childhood injury of broken tibia and large toe

Psych eval - History of depression and post traumatic stress disorder, childhood history indicates emotional and physical abuse

Father - status unknown Diagnosed alcohol use disorder

Brother - deceased, cause of death non-contributory - Substance use disorder

Mother - deceased, cause of death non-contributory - Hypertension, thrombophilia (blood clotting disorder)

Positive family history of hypertension, but no diabetes or cancer

Social drinker - 3-4 glasses of hard liquor each weekend

Smokes socially - 10 pack years

Physically active - Enjoys nightly walks

Psych eval - Other squad members act as his emotional support

Expressed interest in cats and tattoo art (FLAGGED: Further input and comments from other medical professionals would be appreciated)

Medication list + indications

Paracetamol 1000mg - Pain

Amoxicillin/Clavulanic acid 625mg - Infection

Morphine 20mg + Ketamine 4.5mg IV - Pain

Mafenide acetate 5% topical - Antimicrobial, burn wounds

Fluoxetine 20mg twice daily - Depression - not taking est 2001

Allergies

NKDA - No known drug allergies

No environmental, food, or animal allergies

Psych recommends evaluation of a pet, such as cat, for pt while on leave

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tteessiiee · 13 days ago

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Health impacts of obesity, death feedee edition

TW: this is dark and very real, do not read if you are not ready to understand the consequences of feedism. And I really mean it. It may be f* scary.

You know I study physiotherapy at med school. And Im also a feedee, feeder, FA... Which means that mine internships in hospitals are pretty heavy and hard for me. I see all the impacts of obesity, or even morbid obesity on people and their health. On their life.

We are all talking about heart-attacks. Sure, your arteries getting clugged, atherosclerosis growing in your body and getting you closer to an early grave. But atherosclerosis does not cause only heart-attacks. It would be nice, wouldn’t it? Feeling your heart struggling, pain in your chest (which you deserve for being the pig you were), and pretty soon there is the end. Death.

But atherosclerosis can also cause strokes. And I don’t think you want that. Part of your brain gonna die, part gonna live. It can affect your motor functions, your ability to feel by touch, your ability to know where and how placed your limbs are, your speech, of course your ability to think. You may die, sure. Or you gonna survive and live way way worse life fully dependant on people around you… Did you know that?

You also might ruin your pancreas. Im sure that many of you already have insulin tolerance way higher than you should. Well diabetes mellitus is incoming if you will not change your lifestyle. It does not only mean that you will need to take insulin! It will also damage your nerves. Neuropathies are very common. DM can lead even to amputations of legs. And also an impact on eyes is very well known, you can become blind. Over all diabetes is a metabolic disease and it has huge impact on your whole body – nerves, organs, veins, everything.

Another effect of our feedee diet - your liver become fattier making it work less. And liver are very important organ! Liver steatosis can become cirrhosis, the organ will be very damaged. Btw it also gonna increase your blood pressure which has significant impact on probability of heart-attacks and strokes. Another thing – there can appear stones in your gallbladder. That is mainly caused by eating too greasy and fatty food. And this also can be very painful situation needing a surgery.

It is proved that obesity increases the risk of cancer, especially cancer in gastro-intestinal tract and urogenitals. One more thing that people do not want.

Not to mention your musculo-sceletal system. Arthrosis in joints (another painful thing restricting your daily life), unfit and stiff muscles, bones easier to break by your weight if you fall… And it will not hurt only when you move. But also when you lie in your bed getting stuffed to the brim once again. Who of you have never ever had back pain, mainly lower-back pain? It is not comfortable, is it? And it only gonna get worse if you don’t exercise.

There are also impacts on your skin but i'm not good in this field so can't say much about it.

I know it is a lot of fun to be a feedee. To gain, get fatter, heavier, softer. Getting out of breath easily? Oh f* yes please, it makes you so horny. But there is a huge impact on your health. Im sure you know it. But maybe you don’t know all the specific things that may happen. This is just a brief list of health complications that obesity brings. So if you are a death feedee, go on! Eat yourself to these diseases if that’s what you want. But be aware that your life probably will not end by a sudden quick heart attack. You will suffer many months and years due to many comorbidities till your body will give up on you. Are you ready for that long pain?

Wanted to let you know so that I can feel better when I actually encourage you to gain. You know, consent means that you agree while being aware of the consequences. If you want me to help you get morbidly obese I wanna be sure I warned you. And maybe (hopefully) this gonna help someone to stop gaining so much if they find out that they would not be happy. Because babes – I don’t want you fat in the first place. I want you happy.

That’s the reason why im drinking 700 kcal hot chocolate made of heavy cream while writing this article. It makes me happy to gain. It makes me happy being fat even though I know all of these things. And it also scares the s*it out of me. I fear it so much. I want it so much. Im not a death feedee in real life, will not let the kink kill me (I hope). But I definitely am a death feedee in fantasies, deep inside and sometimes it is really hard to find the difference between having fun and ruining your body.

••••••••••••••••••••••••••••••••••••

I warned you it gonna be dark and real 🖤

Enjoy your life as you wish 💕 Give fully into hedonism or enjoy the parts of feedism that don't kill you - that is your choice. Your body. Your life. Your death.

~ Tessie

#dark feedism #dark feederism #death feedism.#death feedee #feedism health #health consequences #health concerns #feedee.#feeder.#feederism.#feedism.#feedee girl #gaining #fatter #getting fat #gaining weight on purpose #feederism health #feedism consequences

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covid-safer-hotties · 2 months ago

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The Long-term Complications of Covid-19 Infection - Published Sept 13, 2024

Context.— As the Covid-19 pandemic continues into its 4th year, reports of long-term morbidity and mortality are now attracting attention. Recent studies suggest that Covid-19 survivors are at increased risk of common illnesses, such as myocardial infarction, diabetes mellitus and autoimmune disorders. Mortality may also be increased. This article will review the evidence that supports some of these observations and provide an opinion about their validity and their relevance to insured cohorts.

Background Many Covid-19 survivors report protracted symptoms, sometimes lasting 3 years or more. These are collectively called post-acute sequelae of SARS-CoV-2 infection (PASC) or long Covid. They have been frequently described.1–4 In the past year, reports of long-term complications such as atrial fibrillation, heart failure, stroke and pulmonary embolism have emerged. In some reports these established disease entities are erroneously described as long Covid, generating confusion. The distinction is important: illness reported in Covid survivors are not restricted to the long Covid cohort. Thus, they are relevant to the majority of the North American population who have been infected by SARS-CoV-2, and not just the estimated 5-10% of individuals who belong to the long Covid cohort. This paper will examine the reports of increased incidence of cardiovascular diseases in both and will examine the reported long-term increase in mortality.

Cardiovascular disease after 1 and 2 years Multiple studies have reported an increased risk of cardiovascular events at 1 year. A February 2022 analysis of 153,760 US veterans, followed for 1 year after Covid-19 infection, reported an increased risk of cerebrovascular disease (HR 1.53), ischemic heart disease (HR 1.66), thromboembolic disease (HR 2.39) and atrial fibrillation (HR 1.71).5 Risk was greatest in those hospitalized and those with pre-morbid illnesses. However, risk was also elevated in outpatients, who constituted the vast majority of the cohort. These findings have been corroborated in 2 further studies. In a 2023 analysis of 690,000 Covid-19 survivors, drawn from the TriNetX database–self-described as the world’s largest global Covid-19 dataset–there was an increased risk of cerebrovascular disease (HR 1.6), ischemic heart disease (HR 2.8), thromboembolic disease (HR 2.6) and atrial fibrillation (HR 2.4) at 1 year.6 In contrast to the VA study which examined a predominantly older male population, the subjects in this study were younger, with mean age 44, and 57% were female. Risk was higher in the >65 age group and was not limited to inpatients. In a May 2023 Lancet retrospective analysis of 535,000 Hong Kong (HK) and 16,000 UK Covid 19 survivors, similar hazard ratios were recorded for stroke (HR 1.2), ischemic heart disease (HR 1.32), atrial fibrillation (HR 1.31) and deep venous thrombosis (HR 1.74).7 However, it is worth noting that while follow-up was described as 28 months for the HK cohort and 17 months for the UK cohort, the median follow-up for the HK group was 146 days and was 243 days for the UK cohort, somewhat limiting the conclusions of true impact at 1 year. Contradicting these studies, a prospective analysis of 17,000 Covid-19 survivors in the UK Biobank, did not document an increased risk of cardiovascular outcomes amongst outpatients, with the exception of thromboembolic disease (HR 2.7).8 An August 2023 analysis of 138,000 VA Covid-19 survivors followed for 2 years– the longest follow-up period to date– reported that the risk of complications in outpatients had returned to baseline at 6 months.9 In contrast, the risk for multiple cardiovascular and thromboembolic complications in the hospitalized cohort remained elevated at 2 years. None of these 5 studies was limited to individuals with long Covid, but similar findings have been reported in this group: a recent analysis of 13,435 individuals who had been diagnosed with long Covid, based on a typical array of symptoms, reported increased risks at 1 year for ischemic heart disease (HR 1.7), ischemic stroke (HR 2.1) and pulmonary embolism (HR 3.6).10

These studies document a fairly consistent, increased risk of cardiovascular complications among Covid-19 survivors. However, important questions remain. Amongst these: does increasing population immunity and vaccination change the risk? Is the magnitude of risk similar for all SARS CoV-2 variants? Does reinfection increase the risk? Answers to some are available. Vaccination appears to attenuate the risk: a Korean study of 592,000 individuals post-Covid-19 infection, showed that vaccination decreased the risk of heart attack and stroke by approximately 50%.11 This finding was replicated in a large US cohort where major adverse cardiovascular events were reduced by a similar amount for full vaccination, and by 25% for partial vaccination.12 Thus, while vaccination does not eliminate long-term complications, it appears to provide a substantial protective effect.

Reinfection may increase the risk of sequelae. In a large US VA cohort of 440,000 Covid survivors, of whom 40,000 had one or more SARS-CoV-2 reinfections, the risk of cardiovascular disorders was increased (HR 3.02), when compared to a single infection.13 Moreover, this risk was not modified by vaccination.

The impact of different variants is less clear. Most of the described studies were conducted in 2020-2021 when delta and pre-delta variants predominated. It is unclear whether similar outcomes would characterize infection with Omicron variants, which remain dominant in most countries since November 2021. Interestingly, the risk of cardiovascular complications in the cohort of Hong Kong survivors described above, where the Omicron was the prevalent strain, was no different than among the comparator UK Biobank cohort, where pre-Omicron strains were prevalent.7

Is there extra long-term mortality after Covid-19 infection? Extra mortality has been reported by several studies.6,8,14–18 A 2021 US analysis of 400 Covid-19 survivors, documented increased mortality (HR 2.5) at 1 year.14 The additional risk was confined to individuals who had been hospitalized. In 2022, 3 studies reported excess mortality in 3 different countries. The first, an Estonian whole-population study of 66,000 Covid-19 survivors, of whom 8% were hospitalized, reported a 3-fold increase in mortality at 12 months.15 Mortality was particularly elevated in the first 5 weeks following infection. For those over age 60, increased mortality persisted until 12 months (HR 2.8). However, for those less than age 60, mortality was not increased after 35 days. The second, an analysis of 690,000 Covid-19 survivors from the TriNetX database also reported increased 1-year mortality risk (HR 1.6).6 This was largely explained by excess deaths in individuals over age 65; below age 45 risk was not increased. For the outpatient cohort the risk of mortality was lower than that of the comparison group (HR 0.46). The third, a study of 25,000 Covid-19 survivors drawn from the UK Biobank, reported increased mortality risk at 20 months, for those with severe Covid infection (HR 14.7), but also an increased risk for those with mild disease (HR 1.23).16 Stratification by age was not provided.

In 2023 4 further studies reported similar, but at times quantitatively different results. Two analyses drew on the UK Biobank cohort. In the first, a prospective evaluation of 7,800 SARS-CoV-2 PCR positive individuals, increased mortality was reported for the study group at 18 months (HR 5.0), when compared to both a contemporary and an historical cohort.17 For the non-severe cases the mortality risk remained elevated (HR 4.8). The second study, already described above– a comparative analysis of 7600 Covid survivors from the UK Biobank and 530,000 Covid survivors in Hong Kong–reported increased mortality (HR 4.16) after 17 months for the former and 28 months for the latter.7 The risk of mortality was higher in the UK than the HK cohort, a difference the authors posited was due to Omicron being the dominant variant in HK during the study period. The risk remained elevated, but less so, for younger cohorts and for mild Covid-19 infections.

Finally, 2 large US studies recently reported mortality at 2 years. In the first, an analysis of 138,000 US veteran Covid-19 survivors with 5.9 million controls, the risk of death for the hospitalized cohort remained elevated at 2 years (HR 1.29).8 In contrast, the risk of death for the outpatient cohort returned to baseline at 6 months. Breakdown of risk by age-group was not provided. The second study, also of US veterans, reported similar findings. In a cohort of 280,000 Covid-19 survivors the risk of death remained elevated at 2 years (HR 2.0).18 The risk was highest in the first 90 days (HR 6.3) and decreased at 6 months (HR 1.18). Thereafter, the risk in Covid-19 survivors was slightly less than the control group (HR 0.89). A post-hoc subgroup analysis examined and refuted the possibility that accelerated mortality in the control group could have explained the lower mortality in Covid-19 survivors. The risk of death in hospitalized individuals remained elevated at 2 years (HR 1.22).

How Plausible is this Information? The studies described above command attention by virtue of their size and the consistency of their findings in different populations, and in different countries. They are also supported by the observations of long-term pathophysiologic abnormalities following SARS-CoV-2 infection, such as ongoing inflammation, persistence of virus, and immune system dysfunction. However, the negative ledger is also substantial. Observational studies such as these, no matter how well-designed, remain open to many types of bias. Reliance on diagnostic codes, prescription records, laboratory results and tallies of clinical visits, to establish disease incidence, is intrinsically error-prone and makes cross-study comparisons difficult. Perhaps more importantly, the cohorts described above were different in many respects, varying from the older, male-predominant cohort of the US VA system to the younger healthier cohort of the UK Biobank. Further, cohorts were constituted during the first year of the pandemic, at a time when healthcare delivery was disrupted, lockdowns were in effect, vaccination and antivirals were largely unavailable, and population immunity levels were low. Thus, it could be argued that the observed outcomes are better explained by an evolving pandemic, rather than solely SARS-CoV-2 infection. This could also explain the most recent reports that after 2 years of follow-up, the risk of both Covid-19 complications and mortality, in most of those infected (i.e., the non-hospitalized), is no longer elevated. It also evident that most of the reported extra mortality is occurring in the early months following infection, where survival curves separate rapidly.6,10,15,18

Are these findings relevant to an insured population? ‘Partially’ is probably the best answer. The most important observation is that hospitalization, and in-particular an intensive care unit admission, is the dominant risk factor for both morbidity and mortality. This risk appears to persist up to 2 years. The second important risk element is the presence of comorbid conditions. This observation raises the interesting question of what exactly causes the extra mortality. Is it due to ‘protracted’ SARS-Co-V-2 infection or is it caused by a recognized complication of Covid-19, such as pulmonary fibrosis or acute kidney injury? Or is it explained by an aggravation of a comorbid illness? Or is it a complication of long Covid? There is a likelihood that all these mechanisms were at play in the cohorts under study.

For non-hospitalized individuals, and those that are healthy, the evidence for extra morbidity and mortality after the first 3-6 months is far from conclusive. For the long Covid cohort, the evidence for additional mortality requires further supporting evidence. As the prevalence of co-morbid conditions is lower in insured populations, one might reasonably expect, based on current evidence, that longer-term morbidity and mortality due to Covid-19 infection will be minimally affected.

References 1.Davis H, McCorkell L, Vogel, J. et al Long COVID: major findings, mechanisms and recommendations. Nat Rev Microbiol 21, 133–146 (2023). doi.org/10.1038/s41579-022-00846-2

2.Meagher T. Long COVID - An Early Perspective. J Insur Med. 2021 Jan 1;49(1):19–23. doi: 10.17849/insm-49-1-1-5.1. PMID: 33784738.

3.Meagher T. Long COVID – One year On. J Insur Med. 2022 Jan 1;49:1–6. doi: 10.17849/insm-49-3-1-6.1. PMID: 33561352.

4.Meagher T. Long Covid - Into the Third Year. J Insur Med 2023;50(1):54–58. doi.org/10.17849/insm-50-1-54-58.1

5.Xie Y, Xu E, Bowe B et al Long-term cardiovascular outcomes of COVID-19. Nat Med 28, 583–590 (2022). doi.org/10.1038/s41591-022-01689-3

6.Wang W, Wang CY, Wang SI et al Long-term cardiovascular outcomes in COVID-19 survivors among non-vaccinated population: A retrospective cohort study from the TriNetX US collaborative networks. eClinicalMedicine. 2022 Nov;53:101619. doi: 10.1016/j.eclinm.2022.101619

7.Lam I, Wong C, Zhang, R et al Long-term post-acute sequelae of COVID-19 infection: a retrospective, multi-database cohort study in Hong Kong and the UK. eClinicalMedicine Vol. 60 Published: May 11, 2023. doi: doi.org/10.1016/j.eclinm.2023.102000

8.Raisi-Estabragh Z, Cooper J, Salih A, et al Cardiovascular disease and mortality sequelae of COVID-19 in the UK Biobank Heart 2023;109:119–126.

9.Bowe, B., Xie, Y. & Al-Aly, Z. Postacute sequelae of COVID-19 at 2 years. Nat Med 29, 2347–2357 (2023). doi.org/10.1038/s41591-023-02521-2

10.DeVries A, Shambhu S, Sloop S et al One-Year Adverse Outcomes Among US Adults With Post–COVID-19 Condition vs Those Without COVID-19 in a Large Commercial Insurance Database. JAMA Health Forum. 2023;4(3):e230010. doi:10.1001/jamahealthforum.2023.0010

11.Kim Y, Huh K, Park Y et al Association Between Vaccination and Acute Myocardial Infarction and Ischemic Stroke After COVID-19 Infection. JAMA. 2022;328(9):887–889. doi:10.1001/jama.2022.12992

12.Jiang J, Chan L, Kauffman J, et al Impact of Vaccination on Major Adverse Cardiovascular Events in Patients With COVID-19 Infection. J Am Coll Cardiol. 2023 Mar, 81(9):928–930. doi.org/10.1016/j.jacc.2022.12.006

13.Bowe B, Xie, Y, Al-Aly Z. Acute and postacute sequelae associated with SARS-CoV-2 reinfection. Nat Med 28, 2398–2405 (2022). doi.org/10.1038/s41591-022-02051-3

14.Mainous AG, Rooks BJ, Wu, et al COVID-19 post-acute sequelae among adults: 12 month mortality risk. Front Med (Lausanne). 2021;8:778434. doi:10.3389/fmed.2021.778434

15.Uuskula A, Jurgenson T, Pisarev H et al Long-term mortality following SARS-CoV-2 infection: A national cohort study from Estonia. The Lancet Regional Health - Europe 2022;18:100394 Published online 29 April 2022. doi.org/10.1016/j.lanepe.2022.100394

16.Xiang Y, Zhang R, Qiu G. et al Association of Covid-19 with risks of hospitalization and mortality from other disorders post-infection: A study of the UK Biobank. medRxiv doi: doi.org/10.1101/2022.03.23.22272811

17.Wan E, Mathur S, Zhang R et al Association of COVID-19 with short- and long-term risk of cardiovascular disease and mortality: a prospective cohort in UK Biobank, Cardiovascular Research, Volume 119, Issue 8, June 2023, 1718–1727. doi.org/10.1093/cvr/cvac195

18.Iwashyna TJ, Seelye S, Berkowitz TS, et al Late Mortality After COVID-19 Infection Among US Veterans vs Risk-Matched Comparators: A 2-Year Cohort Analysis. JAMA Intern Med. Published online August 21, 2023. doi:10.1001/jamainternmed.2023.3587

#mask up #covid #pandemic #covid 19 #wear a mask #public health #coronavirus #sars cov 2 #still coviding #wear a respirator

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jcsmicasereports · 7 days ago

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ABSTRACT

Charcot Arthropathy is a serious complication of Diabetic neuropathy, usually affecting foot or ankle. It causes widespread destruction of affected joints and bones around them leading to severe deformities that may require major amputation. Here, we report the case of a 62 year-old male who presented with severe left foot deformities and swelling on the left big toe that developped over a short period of time. His primary presentation raised the suspicion for a bone tumor or cellulitis which then revealed by X-Ray that it's a Charcot foot necessitating foot fixation, strict glycemic control and treatment with Biphosphonates. This report will therefore serve as a reminder for clinicians to keep in mind Charot Arthropathy in diabetic patients with peripheral neuropathy even if it doesn’t present in a typical manner.

Keywords: Charcot, arthropathy, diabetes, trauma, destruction, joints, deformity, sensation, neuropathy, inflammation, chronic, Fixation, Osteodegenerative, ambulation, uncontrolled.

INTRODUCTION

Charcot Arthropathy is a serious but rare progressive condition that can affect 0.15 – 2.5% of diabetic patients especially those who developed peripheral neuropathy. Despite the voluminous work reported in literature on CA, very few studies mention the prevalence of this disabling disease. The actual incidence of CA may be greater than what is reported, as in many cases, the clinicians fail to diagnose or are late to diagnose this serious complication. Charcot affects the bones, joints, and soft tissues of the foot or ankle. Whilst the exact pathophysiology remains debated, a multifactorial pathogenesis seems likely predominating. This involves repetitive micro-trauma in a foot with impaired sensation and neurovascular changes caused by pathological innervation of the blood vessels leading to bones deformities. Clinical features include signs of inflammation, profound unilateral swelling, an increase in local skin temperature and bone resorption in an insensate foot may be present.

In advanced cases with considerable mid-foot destruction, a typical "rocker bottom" appearance is seen. In most cases, progression of deformity takes a more chronic form and is seen over a period of months, to years.

This case report describes a case of a chronic destructive Charcot foot in a patient with uncontrolled diabetes, which was initially managed as a case of bone tumor.

Case Report

A 62 year old male with a background of Type 2 Diabetes Mellitus, peripheral neuropathy and obesity presented with complain of numbness and decreased sensation of forefoots and a mass in the arch of left foot. Eight days prior, he sustained a fall whilst walking but denied any injury, swelling or pain at that time. He said his left big toe was totally straight but now has deformed (into Morton) and his 2nd toe looks bigger due to big toe deformation and often remains bend in shoes which he doesn’t feel, but when removing the shoes he often finds it bent. The patient denies any pain in the deformed toe but a little feeling of warmth in the pathological area.

Examination revealed a warm, swollen left foot with a 2 mm healing ulceration on the plantar surface and a lumpy sensation on the left big toe. Blood tests showed normal white blood cells count, elevated C-reactive Protein (CRP-67) and a thrombocytosis. His fasting blood glucose level was 221 mg/dl with features of uncontrolled diabetes.

Plain film X-Ray revealed complete fracture dislocations of the 1st , second and fifth tarsometatarsal joints with large bone deformity on the left arch of the foot as well as another deformity on the right arch and lower calcaneus {Figure.2}. This was correlated with bone CT (computed tomography) and MRI (Magnetic Resonance) imaging, with interval changes noted to be of chronic onset.

Discussion

Charcot foot is a well-documented complication of diabetic neuropathy. The mechanism of this is not fully understood but two theories exist – namely, the neurovascular and neurotraumatic theories. In the neurovascular theory, an underlying autonomic neuropathy leads to hypervascularity, osteolytic changes and demineralization. However, the neurotraumatic hypothesis indicates that unperceived trauma to an insensate extremity leads to continued bony destruction on ambulation, which worsens and progresses. These theories imply that a sufficient time frame is required for established Charcot foot destruction to develop.

Typical progression of Charcot foot occurs over months to years, although rare acute onsets have been reported. However, the progression seen in our patient, from normal X-Ray appearances to established, acute Charcot foot with considerable mid-foot destruction over a period of just 10 days is a rarely described progression of Charcot arthropathy. The combination of local skin warmth with decreased sensation in the left foot and feeling of a bony lump on the left arch raised the suspicion of a bone tumor, but X-Rays as well as CT Scan of the foot beside the uncontrolled diabetes in this patient made Charcot foot a more possible diagnosis.

Early recognition of Charcot Arthropathy is a mandatory to ensure improved outcomes. It is important to differentiate between acute Charcot foot, infection and bone tumors through clinical investigations as well as patient medical history. The presence of ulcers should raise the suspicion of infection or osteomyelitis, and therefore, the importance of early imaging cannot be overstated. Modestly raised inflammatory markers (CRP-68) in this diabetic patient along with left foot deformities suggest an acute Charcot foot than an infectious process. The latter frequently presents with high laboratory values.

The initial management of the patient was fixation with a total contact leg cast, followed by open reduction and internal fixation (ORIF) with locking plates, combined with lengthening of Achilles tendon to permit full dorsiflexion and subsequent re-casting.

Due to osteodegenerative nature of CN, all attempts at pharmacological treatment have focused on anti-osteoporotic drugs so we started the patient on an Alindronate beside a more strict control of his diabetes. His post-operative progress was satisfactory and he is currently non-weight bearing for 6 months post-ORIF.

Conclusions

The case highlights an important clinical scenario that can be misdiagnosed in a diabetic patient. A clinical presentation of unilateral foot swelling, erythema, warmth and decreased sensation should raise suspicion for Charcot Arthropathy even in the absence of trauma history. I hope this will be a helpful reminder to clinicians when dealing with similar presentations.

#Charcot #arthropathy #diabetes #trauma #destruction #joints #deformity #sensation #neuropathy #inflammation #chronic #Fixation #Osteodegenerative #ambulation #uncontrolled #jcrmhs #Journal of Clinical Case Reports Medical Images and Health Sciences submissions

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diabetes-health-corner · 5 months ago

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Long term Complications of Diabetes Mellitus

Failure to control blood sugar will damage the body’s blood vessels, and this damage leads to complications of diabetes. These problems do not happen overnight, but their very insidious nature makes them all the more dangerous.

Read the full blog: https://www.freedomfromdiabetes.org/blog/post/long-term-complications-of-diabetes-mellitus/394

#Complications of Diabetes Mellitus #complications of diabetes #complications of diabetes mellitus #type2 diabetes complications #long term complications of diabetes #microvascular complication of diabetes #number one complication of diabetes #chronic complication of diabetes mellitus #what is complication of diabetes #short term complication of diabetes #most common complication of diabetes #the most complication of diabetes

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viasox · 6 months ago

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#carbohydrates #diabetic friendly #diabetes mellitus #health #diabetic neuropathy #diabetes complications #healthy diet #sugarcontrol #type 2 diabetes

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cbirt · 2 years ago

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Scientists Unveil High-Resolution Reference Genome of Nile Rat – A Promising Animal Model for Diabetes Research

A research team from the Morgridge Institute for Research has put forth a reference genome with haplotype-resolved assemblies and gene annotations deciphering the Nile Rat (Arvicanthis niloticus) as a carbohydrate-sensitive model for diabetes research.

An animal model is a living, genetically engineered organism used for research and investigating human diseases. Animals such as mice, rats, flies, worms, zebrafish, etc., are widely used to understand the genetic underpinnings and behavioral analysis of pathological conditions. Researchers have found significant molecular mechanisms in biological processes relevant to human health thanks to the high-throughput genomes of the house mouse (Mus musculus) and Norway rat (Rattus norvegicus). However, even frequently used nocturnal animal models do not adequately represent a wide range of human features.

With mice and rats being nocturnal, it is not the perfect model to study human circadian cycles (studies have shown that circadian disruption impairs pancreatic beta cell function and insulin sensitivity, which results in impaired glucose tolerance). Although a high-fat diet can also cause these models to experience pre-diabetic symptoms, they hardly ever experience long-term diabetic consequences like people with the illness do. No single animal model has shown the capability to mirror the complications of long-term human diabetes mellitus.

#bioinformatics #genomics #genome #ngs #scicomm #diabetes #stem #sequencing

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sosata7 · 5 months ago

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The Prevention, Treatment, and Complications of Diabetes Mellitus

free download click here

#suger control #suger defender #health and wellness #sugerdaddy #blood suger balance

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puppyexpressions · 1 year ago

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Diabetes in Dogs

Even dogs eating healthy diets can suffer from diabetes. As with diabetes in humans, sometimes a dog’s body’s stops producing enough insulin or the cells of a dog’s body are unable to use the insulin that is produced. When either condition occurs, the result is diabetes mellitus, which causes excessive thirst and urination and extreme hunger accompanied by weight loss. To stabilize sugar levels, insulin therapy is the treatment at the outset and is usually required for the life of the dog.

Symptoms and Identification

Excessive thirst and urination: This happens because the huge quantity of sugar in the bloodstream spills into the urine and pulls water out of the bloodstream along with it, thereby causing increased urine production and urination. Increased drinking is the body’s way of trying to compensate for increased water loss through urination. Due to the high levels of bacteria-attracting sugar in the urine, urinary tract infections are also a routine finding.

Appetite increase paired with weight loss: This happens because when sugars cannot enter cells, the body is unable to effectively use the food it takes in as energy. Hunger is never satisfied despite a typically ravenous appetite, and weight loss is almost always a feature.

Other symptoms may include:

Urinary accidents in the house

Vomiting

Dehydration

Lethargy (tiredness)

Veterinarians may suspect canine diabetes if any suspicious clinical signs, such as increased drinking and/or urinating, have been observed at home. After performing a thorough physical examination, your veterinarian may recommend some of these tests to help confirm a diagnosis:

CBC (complete blood count) and chemistry profile: When a pet is ill, these tests are commonly performed together during initial blood testing to provide information about the pet’s organ systems. The CBC and chemistry profile may show dehydration, an elevated blood sugar level, or other changes that can occur with diabetes.

Urinalysis: Evaluation of a urine sample may show the presence of sugar (glucose) in the urine if a dog has diabetes.

Fructosamine: Fructosamine is a protein in the blood that binds very securely to glucose. The fructosamine level is therefore a close estimation of the blood glucose level, but it is less likely to change due to stress and other factors that affect the blood glucose level. Additionally, the fructosamine level indicates where the blood sugar levels have been during the previous two to three weeks. In a dog with diabetes, the blood sugar levels are usually high for long periods of time, which would be reflected by an increased fructosamine level.

Affected Breeds

Predisposed breeds include the Miniature Schnauzer, Standard Schnauzer, Poodle, Australian Terrier, Spitz, Bichon Frise, Samoyed, and Keeshond. Dogs of any breed, however, may acquire diabetes.

Treatment

In the long term, dogs with diabetes are often treated by insulin injection to help the body’s needy cells use sugar more efficiently. Dietary changes can also help, by tempering sudden spikes in blood sugar levels. Insulin injections, however, are generally started at the time of diagnosis and required long term to control the disease.

In the short term, some patients require hospitalization. Some may even need intensive care should their presentation be complicated by a variety of other problems secondary to the diabetes (this is a common scenario).

After treatment begins, periodic blood and urine tests are generally recommended. This helps ensure that the insulin dosage is right for your dog. Your dog’s weight, appetite, drinking and urination, and attitude at home can all provide useful information that helps determine if his or her diabetes is being well managed. Your veterinarian will consider all of these factors when making recommendations for continued management.

Many dogs live active, happy lives once their diabetes is well regulated. However, insulin therapy and regular monitoring at home and by your veterinarian are necessary for the rest of your dog’s life.

Prevention

Keeping your dog at a healthy weight can help reduce his risk of developing diabetes. However, for dogs that are genetically predisposed, their risk for developing disease remains higher even if they maintain a healthy weight.

#diabetic dogs #dogs and diabetes #diabetes

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