#splenomegaly

[biology-geology-beaches-india]

The Research Journals of Satyendra Sunkavally, page 34.

[drforambhuta]

I. Polycythemia Diagnosis:

A. Clinical Assessment:

• The diagnostic process for polycythemia commences with a thorough examination of medical history and physical condition to detect signs indicative of erythrocytosis, assess potential risk factors (e.g., smoking habits, family history of thrombosis), and uncover underlying causes.

• Special attention should be given to symptoms of hyperviscosity syndrome (e.g., headaches, dizziness), skin manifestations (e.g., erythromelalgia), and signs of organ enlargement (e.g., splenomegaly, hepatomegaly).

B. Laboratory Tests:

• Laboratory investigations are crucial for diagnosing polycythemia and understanding its underlying mechanisms. Essential tests include a complete blood count (CBC) with differential, examination of peripheral blood smear, and measurement of serum erythropoietin levels.

• Additional tests, such as JAK2 mutation analysis, bone marrow biopsy, and molecular testing for other mutations associated with myeloproliferative neoplasms (e.g., CALR, MPL), may be necessary to confirm the diagnosis of PV and rule out alternative causes.

C. Imaging Techniques:

• Imaging methods like ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI) may be used to evaluate organ enlargement (e.g., splenomegaly, hepatomegaly) and identify potential underlying factors for secondary polycythemia (e.g., renal tumors).

II. Polycythemia Treatment:

Management of polycythemia aims to alleviate symptoms, lower the risk of thrombotic complications, and prevent disease progression. Treatment approaches may vary depending on the underlying cause and severity, often involving a combination of strategies:

A. Phlebotomy (Venesection):

• Phlebotomy is the primary treatment for PV, involving the removal of excess blood to achieve target hematocrit levels (<45% in men, <42% in women).

• Regular phlebotomy sessions usually start at diagnosis and are adjusted based on individual response and disease activity.

B. Cytoreductive Therapy:

• Drugs like hydroxyurea, interferon-alpha, and ruxolitinib may be used in PV patients who do not respond to or cannot tolerate phlebotomy.

• These drugs work by suppressing abnormal hematopoietic proliferation and reducing the risk of blood clotting, with hydroxyurea being the most commonly used and studied cytoreductive drug in PV.

C. Antiplatelet Therapy:

• Aspirin and other antiplatelet drugs are often prescribed to PV patients with a history of blood clots or other high-risk factors to lower the risk of arterial thrombosis.

• Aspirin is usually started at low doses (e.g., 81 mg daily) and may be combined with cytoreductive therapy for better thromboprophylaxis.

D. Treating Underlying Conditions:

• Management of secondary polycythemia focuses on addressing the root cause to relieve hypoxia-induced erythropoiesis and prevent disease progression.

• Interventions may include oxygen therapy for patients with chronic respiratory problems, correction of hemoglobin disorders or other genetic issues, and surgical removal of erythropoietin-secreting tumors.

E. Lifestyle Changes:

• Lifestyle adjustments such as quitting smoking, maintaining a healthy weight, regular physical activity, and proper hydration are vital for improving clinical outcomes and reducing cardiovascular risks in polycythemia patients.

Doctors suggest undergoing regular health checkups for the early diagnosis and treatment of polycythemia. You can choose to undergo a regular full body health checkup at Jaslok Hospital Mumbai, which is one of India's best hospitals for the early detection and management of blood disorders.

[kaizenhospitals]

Exploring Effective Treatments for Spleen Diseases

Discover comprehensive approaches and innovative therapies for managing various spleen diseases. From conventional medical interventions to emerging treatments, learn about options to improve patient outcomes and enhance quality of life. Explore the evolving landscape of spleen disease treatment strategies and their potential impact on patient care and well-being.

[chrissy-kaos]

**Health update**

So I never wanted to make another post like this but here I am.. I was hoping to just get better and never bring it up again.

To get those of you up to speed. I was diagnosed with CKD back in late 2021. I’ve been battling that for a while now. I’m actually doing really well in that regard. During a routine MRI in Nov 2023 for my kidneys we found what looked to be a hepatic steatosis and splenomegaly. It was later determined and I was diagnosed with hepatic tumors and splenomegaly. I also had a fairly large gallstone and what appeared to be a tumor/cyst on my gallbladder. We decided it was just better to remove my GB and the tumors all at the same time. So in January of this year I had laparoscopic cholecystectomy/tumor removal. That’s what the scars on my stomach are from. The tumors were tested and were benign. That was a huge relief. But it left my liver fairly damaged. I wasn’t to concerned about because your liver can and will heal itself. I recovered well and felt great.

Fast forward 9 months. I wasn’t feeling very well. So I made an appointment with my PCP and she wanted me to do a bloodwork panel. This is normal. We actually do blood once a month but really only check kidneys, thyroid, and hormones. So I did the panel and when the test results came in my Dr called me immediately. She ordered another AST/hepatic function panel for my liver, kidneys and pancreas.

After those test results came in she had me come to her office. I was met with her and a Hepatologist. They broke the news to me that unfortunately my liver not doing well according to the bloodwork. My pancreas/kidneys are actually pretty ok rn which is cool. But my total bilirubin is 1.4 mg/dl. At 1.5 mg/dl total bilirubin is where we really start looking at the possibility of Cirrhosis. If you don’t know what that is. Google it. Now I’m not saying I have this rn but it seems to be looking that way 🫤

They were telling me they could see my bilirubin trending up over the course of the past few months of bloodwork. Also previously being diagnosed with Splenomegaly which is a tell tale sign of Cirrhosis apparently. They’re pretty sure I have it or will have it. They want to run more tests and see how bad or good it is and we’ll go from there. It seems like they have a pretty good plan. Also for those of you that are going to say get a second opinion.. I got a second and a third. They said the same thing go figure..

So again I find myself going in and out of the hospital again. I don’t wish this life upon anyone. It’s not fun. Being chronically/terminally ill is no fucking joke. If it’s not one thing it’s another. It’s tiring and I’m soo tired. Honestly I can’t wait until it’s all over.. forever.

Anyway I figured I’d give you a bit of an update on my health and such. A lot of you ask in my DMs. It’s hard to answer everyone so a post like this gets it out there. But yea if you made it this far thank you and I love you 🫶🏻

[justkidneying]

Why the Spleen Sucks

The spleen is a really shittily placed organ, making it prone to injury. This injury is usually severe and can lead to death if not properly managed. We're going to look at the function of the spleen, what happens when it is damaged, and how to write about.

Where is the spleen? It's in the upper left quadrant of the abdominal cavity, nestled right against the ribs (typically 9-11) at the midaxillary line. It's behind the stomach and is considered intraperitoneal. The main thing is that the spleen is very vulnerable. It is literally right up against the ribs without much protecting it. It's shaped like a little bean and is purple in humans. It is fed by the splenic artery, which comes off of the celiac trunk (which sticks off of the abdominal aorta).

What does the spleen do? Its main job is to filter out old and malformed red blood cells. It also holds immune cells. Certain diseases can cause the spleen to enlarge, including cirrhosis of the liver (it's connected to the hepatic portal system), sickle cell anemia (RBCs are stuck in it), and autoimmune disorders. The spleen also holds about 250 mL of RBCs in reserve in case you need them.

What happens when it is injured? The spleen can be ruptured and lacerated kinda easily. Blunt trauma to the ribs can cause it to rupture, and this is seen in contact sports and car accidents mostly. Because of those giant gaps between the ribs, it's also prone to injury from knife attacks. Gunshot wounds are another common cause, as well as broken ribs penetrating it (broken ribs are very sharp, like way sharper than you imagine). Rupture is more likely when someone has splenomegaly.

When the spleen is damaged, you're going to get a lot of intraperitoneal hemorrhaging. The spleen filters a lot of blood and has blood in it, so there's going to be a lot of blood in the abdomen (obviously). This will lead to distention, guarding (abs are tense), and hypovolemia. The left upper quadrant will be painful, and there can also be referred pain to the left shoulder (Kehr's sign).

If the patient has a small laceration, the symptoms aren't always as dramatic. Sometimes they'll just have low hemoglobin (which is on RBCs), maybe some thrombocytopenia (lots of platelets in the blood).

How do you fix this? If the injury is small and the patient is hemodynamically stable, they can usually be given a blood transfusion and the spleen can heal itself. Sometimes surgery is also performed to clamp a vessel or repair the outer layer of the spleen.

If the injury is major, then surgery will be performed. If the patient is less critical, they may go in and try to fix the problem. If it can't be fixed, they may do a splenectomy (remove the spleen). In a critical patient, they might forgo the nice pretty incision on the left side, and instead just split the patient down the middle. In these situations (in my experience), there isn't a lot of time to waste. One thing that we aren't going to waste time on is anesthesia, for example. This is with a lot of very critical surgeries, at least from what I have seen. Like the surgeon will start cutting as they are working on knocking out the patient, but usually they are in so much pain that they don't even register it.

If you remove the spleen, the patient is more at risk for infections, but with modern medicine and vaccinations, it's not as much of a big deal as it used to be. The patient will probably be fine.

Writing tips: (new section idea, hope you guys like it, lol) As with any injury, you have to make sure that you are giving them an acceptable mechanism of injury. With the spleen, this is either blunt trauma or penetration/laceration. Getting tackled, getting stabbed, getting shot, all great MOIs.

Second thing, present the appropriate signs and symptoms. A sign would be like bruising, hypotension, tachycardia, etc. A symptom would be LUQ pain, Kehr's sign, etc.

Next, figure out what you're going to do and where you're going to do it. In the field, there probably isn't much you can do. The most would probably be a laparotomy and clamping the splenic artery, but I mean, when I was an EMT, we were not doing this. There's a lot of stuff you can theoretically do, but never gets done. But I mean you can write it. If the patient makes it to the hospital, I think it would be more fun to do emergency surgery and just split them right down the middle. There's going to be a lot of blood in the greater omentum, very high stakes and exciting.

Anyways, hope you guys liked this, please let me know if I got anything wrong. I wrote this off of my personal experience and a few good textbooks, but there can always been mistakes in things.

[flyonthewallmedstudent]

Q Fever

Aka, Query fever. What a weird name for a disease. Imagine telling people that's what you got.

in the 30s-40s, an Australian pathologist in QLD/Brisbane, came across an outbreak of the same or similar illness among abbatoir or slaughterhouse workers.

At the time, he called the disease "Q" fever or query as a temporary name until the pathogen could be identified. Unfortunately it stuck.

decades later, now nobel prize winner and virologist, MacFarlane Burnett isolated and identified the microbe responsible. I think this discovery contributed to his prize. i forget already.

Microbe responsible: Coxiella burnetti. Named for Burnett and HR Cox, the American bacteriologist who found the genus Coxiella where C burnetti falls under.

Initially they felt it was related to Rickettsia, responsible for Rocky Mountain Spotted Fever, but as science progressed, this was disproven.

Now for a Case Report

A 55 yo Italian man with a history of aortic valve replacement was diagnosed with pyrexia of unknown origin twice. Further signs included myalgias/splenomegaly/night sweats. The 2nd time he was admitted for PUO he deteriorated rather dramatically and was put on meropenem and teicoplanin.

A host of organisms was tested for on serological testing based on the man's travel and epidemiological history, all negative. Even a rheumatological panel was done, also less revealing. He also had a history of MGUS (a haem disoder), which is kind of a red herring here.

Cultures were negative, no vegetations were seen on a TTE - so they did consider IE. Which is an important differential for PUO.

Eventually a PET-CT was done (often favoured when investigations do not yield much for a sick patient with fevers), finally revealing a focus of infectious on his ascending aorta, where he'd also had previous surgery done. And in a round about way, they also further identified Coxiella Burnetti. He was treated doxycycline and hydroxychloroquine. As it's so rare in Italy, it wasn't really considered even though he mentioned rural travel.

Bottomline: Q Fever is an important consideration in the work up for culture negative IE. Further to this, always consider IE in the differentials for PUO particularly if they're at increased risk for IE (prosthetic valves, damaged valves, select congenital heart issues, previous IE). IE can present with night sweats, fevers, weight loss and splenomegaly. It can be insidious and chronic in nature. other risk factors can be more suggestive as we'll get into below.

Causative organism

Coxiella burnetti, it's a zoonoses - i.e. transmissible from animals. Special powers: very tough/hardy, can survive extreme environments (high temps and UV light etc.) over prolonged periods and is resistant to many common disinfectants/surface cleaners.

It's an intracellular pathogen and gram negative coccobacilli (PINK!)

name coccobaccili reminds me of cocopuffs.

it's mainly associated with farm animals, which the CDC so wholesomely displays on its website on Q fever (wtf).

goats, sheep, cattle typically (but many other animals, even birds, dogs and horses can be reservoirs)

in particular bodily fluids - amniotic fluid, placenta, faeces/urine, milk etc.

you can get it through unpasteurized milk and through inhaling it if it lands on dust in the area

ever visit a farm or petting zoo lately? OMG WASH YOU HANDS.

That said, it's typically inhaled in inorganic dust. You inhale it, it goes to the lungs, and then the bloodstream.

Increased risk for Coxiella burnetti (What to take on history of exposures and when to strongly consider it)

live on a farm or near one

exposure to a farm

work as a vet on a farm

farm worker, dairy workers, researchers on these animals/facilities

slaughterhouse/abbatoir

Also from CDC:

Clinical presentation

Most won't get sick after exposure and remain asymptomatic, a very small minority does. even though it is highly infectious.

incubation time is 2-3 weeks (consider this time in your history of exposure, did they work on the farm 2-3 weeks ago as opposed to yesterday).

Nonspecific acute infectious symptoms:

nonspecific systemic fevers/malaise/arthralgias/myalgias--> key is high fevers though and can be associated with headache and photophobia.

non specific GI - N/V/diarrhoea

respiratory ones - SOB or cough, consider it as atypical cause of community acquired pneumonia.

rare: hepatitis and jaundice (granulomatous) or encephalitis with neurological complications such as demyelinating disease or CN palsies, also haemolytic anaemia and HLH (yikes)

really it's the history of exposure that will lead you down the garden path to Q fever.

Chronic Q fever is perhaps worse, and can present as culture negative IE/PUO. Months/years later, as B symptoms as above above + LOW/LOA, night sweats. More likely to occur if you are predisposed for IE as above, have a weakened immune system for any reason, including pregnancy.

Chronic Q fever has a mortality of 10% if left untreated. About <5% of those with acute Q fever develop this if left untreated. Speculation is that it's more of an autoimmune process or abnormal immunological response to the bacteria.

To be honest, most who walk in the door with community acquired pneumonia get treated empirically for atypicals anyway, (standard course of doxycycline), so we hardly really ponder the question of Q fever in every patient. But if they present chronically and did not have atypical cover at the onset of acute symptoms, then it's something important to consider.

Other important conditions - can cause complications in pregnant women and 20% will get post Q fever syndrome. like chronic fatigue.

investigations

Serology! nice and easy. Look for IgG antibodies in the chronic presentation. Or PCR. Down side to serology - can take 2-3 days for the body to make said antibodies to the bacteria for detection. PCR can be done on any fluids/tissue sent.

Cultures useless, hence it fall under the umbrella of culture negative (hard to grow outside a host cell, it is an obligate intracellular pathogen).

Other hints on bloods (as serology/PCR takes time to return) - elevated or low platelet's, transaminitis with normal bili, opacities in CXR with hilar lymphadenopathy, CSF will show raised protein levels if done when encephalitis is suspected.

imaging can also support the diagnosis.. as illustrated by the case report.

Treatment

Acute disease - as standard for atypical bugs, doxycycline 100 mg BD for 14 days. Alternatives - TMP SMX or Clarithromycin.

Chronic Q fever or IE:

native valves: doxycycline and hydroxychloroquine (200 TDS) for 18 months

prosthetic: same but 24 months

why hydroxy: enhances the action of doxycycline (increases the pH of the phagolysosome)

Follow-up: look for 4 fold decrease in IGG

Sources:

CDC

Stat Pearls

Wiki as linked above

[covid-safer-hotties]

Reference archived on our website

Abstract

Objective COVID-19 induces the development of autoimmune diseases, including SLE, which are characterised by inflammation, autoantibodies and thrombosis. However, the effects of COVID-19 on SLE remain unclear.

Methods We investigated the effects of COVID-19 on SLE development and progression in three animal models. Plasmids encoding SARS-CoV-2 spike protein and ACE2 receptor were injected into R848-induced BALB/C lupus mice, R848-induced IL-1 receptor antagonist knockout (KO) lupus mice and MRL/lpr mice. Serum levels of albumin and autoantibodies, lymphocyte phenotypes and tissue histology were evaluated.

Results In R848-induced BALB/C lupus mice, the SARS-CoV-2 spike protein increased autoantibody and albumin levels compared with vehicle and mock treatments. These mice also exhibited splenomegaly, which was further exacerbated by the spike protein. Flow cytometric analysis revealed elevated T helper 1 cell counts, and histological analysis indicated increased levels of the fibrosis marker protein α-smooth muscle actin. In KO mice, the spike protein induced splenomegaly, severe kidney damage and pronounced lung fibrosis. In the MRL/lpr group, spike protein increased the serum levels of autoantibodies, albumin and the thrombosis marker chemokine (C-X-C motif) ligand 4.

Conclusion COVID-19 accelerated the development and progression of lupus by inducing autoantibody production, fibrosis and thrombosis.

[wheelie-sick]

having the hEDS trifecta + lupus is very frustrating because it's just like "okay where is this symptom coming from?" and no doctor can agree so it doesn't get treated

I have professionally diagnosed MCAS

I'd like to share the symptoms of MCAS can cause:

Constitutional : Fatigue, subjective hyperthermia and/or hypothermia, sweats, change in appetite, weight gain/loss, chemical/physical sensitivities, poor healing

Dermatologic : Urticaria, itch, flushing, hemangiomas with itch/pain, various rashes, telangiectasias, striae, skin tags, folliculitis, ulcers, eczema, angioedema, alopecia, onychodystrophy

Ophthalmologic : Irritated, “dry” eyes, difficulty focusing, blepharospasm

Otologic : Tinnitus, hearing loss, coryza, rhinitis, nasal congestion, epistaxis

Oropharyngeal: Pain, burning, leukoplakia, ulcers, angioedema, dysgeusia, dental and/or periodontal inflammation/decay

Lymphatic: Lymphadenopathy, rare splenomegaly

Pulmonary: Dry cough, dyspnea (difficulty taking a deep breath), wheezing, obstructive sleep apnea

Cardiovascular: Presyncope, hypertension, blood pressure lability, palpitations, edema, chest pain, allergic angina (Kounis syndrome)

Gastrointestinal: Dyspepsia, gastroesophageal reflux, abdominal pain, nausea, vomiting, diarrhea and/or constipation, gastroparesis, angioedema, dysphagia (usually proximal), bloating (post-prandial or spontaneous), malabsorption

Genitourinary: Menorrhagia, pelvic pain, endometriosis, vulvodynia, vaginitis, dysmenorrhea, miscarriages, infertility, dysuria

Musculoskeletal: Myalgias, migratory bone/joint pain, osteopenia/osteoporosis

Neurologic : Headache, migraine, sensory neuropathies, dysautonomia, episodic weakness, seizure disorders, non-epileptic seizures, cognitive dysfunction, insomnia, hypersomnolence, restless leg syndrome

Psychiatric: Depression, anger/irritability, mood lability, anxiety, panic, obsession–compulsion, attention deficit/hyperactivity

Hematologic: Easy bruising, polycythemia, anemia

Immunologic: Hypersensitivity reactions, increased risk for malignancy and autoimmunity, impaired healing, increased susceptibility to infection

source

"well that's just everything" ya. that's why I can't figure out where my symptoms are coming from. lupus is also like this. autonomic neuropathy is also like this. my doctors run in circles pointing at the other doctors to solve the problem but none of them want to.

[jcsmicasereports]

Coinfections and pulmonary embolism in a patient with onset of Leukemia concomitantly with COVID19- Case report by Evgenia Papakonstantinou in Journal of Clinical Case Reports Medical Images and Health Sciences

Abstract

The pandemic of COVID19 is ongoing, with the treatment of neoplastic diseases to be challenging. Patients with acute leukemia are vulnerable to many pathogens due to impaired immunity coming from their disease and simultaneous chemotherapy. Although the COVID19 disease evolves milder in children, concomitant treatment for leukemia may be fatal. We present a girl with COVID19 and Escherichia Hermannii infection at diagnosis for Acute Lymphoblastic Leukemia (ALL). This child suffered bilateral pulmonary embolism after initiation of treatment. We discuss the therapeutic challenges about the initiation of chemotherapy in the context of coinfections as well as the role of COVID19 and other predisposing factors to pulmonary embolism. We found that the slight delay in the antineoplastic treatment contributed to the remission of the acute infection and did not negatively impact the initial response to the leukemia treatment. Nevertheless, the resumption of the oncological treatment should remain among our priorities.

Keywords

Acute leukemia, COVID19, Escherichia Hermannii, pulmonary embolism

Introduction

Given the immunodeficiency due to their disease and chemotherapy, patients with cancer are vulnerable to infections and COVID19 infection is really threatening. We describe a successful management of a girl diagnosed with acute lymphoblastic leukemia (ALL) and COVID19 infection concomitantly with Escherichia Hermannii sepsis. The initiation of chemotherapy was slightly postponed, due to the danger of these severe infections until blood cultures were negative for E. Hermanii. Pulmonary thrombosis was added, as COVID-19 infection predisposes for developing cardiovascular complications, while our patient was under existing predisposing factors for thrombophilia, but with appropriate management had successful outcome.

Case History

A three-year-old girl who presented with a four-day fever, rhinitis, and cough, found positive for COVID19 infection without mutation, as all her family members. She had anemia (Hb: 2.9 g/dL), neutropenia (N: 371/μL), thrombopenia (PLT: 24 K/μL) while tachypnea (RR=31/min), tachycardia (HR=146/min), fever 38.6°C, air oxygen saturation 97%, were found on examination. Empirical antimicrobial treatment with Tazobactam-Piperacillin, Amikacin, Teicoplanin, and Micafungin were given for febrile neutropenia, transfusions (blood, platelets) for myelosuppression, Remdesivir (5 mg/kg) for COVID19. Blood culture yielded Escherichia Hermannii sensitive to receiving antibiotics, but therapy was upscaled to Meropenem due to elevated CRP (109mg/l) and persistent fever 40.6°C. The antibiotic treatment lasting 14-days ceased after two negative cultures. Baseline chest computed tomography (CT) scan showed small cloudy glass spots, areas of pulmonary thickening, atelectasis. Bone marrow aspiration, with 61% blasts, set the diagnosis of pre-B acute lymphoblastic leukemia (ALL) hyperdiploid, Central Nervous System (CNS) negative. Abdominal ultrasound showed hepatomegaly and splenomegaly. Examinations for thrombophilia revealed heterozygosity for factor V Leiden. Chemotherapy started while positive for COVID according to ALLIC 2009 protocol, standard risk arm, 15 days post diagnosis. Remained in COVID clinic until two negative PCR tests. The ALL re-examination showed good prednisolone response on Day 8, complete remission on Days 15, 33. On Day 40 from the initiation of chemotherapy, she had tachypnea with a value of D-dimer elevated at 2.145 ng/mL. Chest CT revealed subsegmental pulmonary embolism on both lower lobes of the lungs. She had not high oxygen requirements, hemodynamic instability requiring intubation, and was treated with low molecular weight heparin for 3 months. She continued chemotherapy without delays, with regular weekly tests for COVID19 and without reactivations, despite the use of corticosteroids and immunosuppressive therapy.

Discussion

The management of children with haematological malignancies and Sars-Cov 2 infection remains challenging since limited data about the impact of COVID 19 in these children are available. Main goal is to optimize the oncological treatment and avoid severe Sars-Cov2 infection due to immunosuppressive therapy. The Escherichia Hermanni bacteremia1 at diagnosis increased the risk of severe complications and led to slight delay of the chemotherapy initiation. The risk of virus transmission to the immunocompromised children in our department required a structured protocol regarding nursing care and isolation techniques. According to American Society of Hematology guidelines2, (January 2021), treatment for ALL patients is individualized, especially during the induction period. Reducing chemotherapy doses is not recommended since it may alter the expected therapeutic effect on ALL, while the severity of COVID19 does not seem to be affected. According to SFCE3 (French Society Committee for fight children and adolescents' Cancers), the main threat to children with ALL remains the ALL itself, even if life-threatening infections are emerging. We slightly delayed the chemotherapy initiation and prioritized treating the viral and bacterial infection since the type of leukemia of our patient was neither potentially life-threatening nor high risk (WBC<20.000, no HR cytogenetic findings, no CNS involvement). Our concern was that the co infections could be deteriorated if we had started induction chemotherapy and corticosteroids. The limited data available suggest a significant heterogeneity regarding the time till the first negative COVID19 PCR test in oncology patients (from four to 94 days). Bisogno et al. reported 19 patients with a mean time to negative PCR of 22 days and eight patients with 19 days4. Our patient demonstrated negative PCR testing for Sars-Cov2 on the 40th day of chemotherapy. As there is no standard therapy established for paediatric oncology patients with COVID19 yet, many centers follow the treatment strategy as in adults. Bisogno et al. treated nine out of 29 oncological patients suffering from COVID19 with Ritonavir, Hydroxychloroquine, and immune plasma. The Children's Hospital of Philadelphia (CHOP) reported their experience with the plasma administration to critically ill children5. Remdesivir is RNA polymerase inhibitor recommended in children with severe Sars-Cov2 infection and underlying medical conditions, especially in the early course of illness. According to a recent meta-analysis remdesivir has the most promising evidence that improves the time to recovery6. In our patient the seven-day lasting antiviral therapy was well tolerated, without any pathological findings. The reported cases of venous thromboembolism may be related to the systemic inflammatory response or a state of hypercoagulability8. Our patient had multiple coexisting risk factors predisposing for thrombophilia, such as administration of Asparaginase, use of a central venous catheter (Hickman), and heterozygous status for the factor V Leiden. In patients with ALL and COVID19, prophylactic administration of anticoagulants may have an impact, but there are not yet standardize recommendations. We need to maintain a high index of suspicion for pulmonary embolism in patients with COVID19 and leukemia and to measure D-dimers regularly. There is need for guidelines for prophylaxis with low molecular weight heparin for pulmonary embolism in patients with COVID-19 and existing risk factors for thromboembolism. The patient was treated successfully with three- month administration of low molecular weight heparin. She continued chemotherapy without delays, with regular weekly tests for COVID19 as some authors have reported reactivations, without reactivations, despite the use of corticosteroids and immunosuppressive therapy.

Acknowledgements

Dr Pappa A., Medical Biopathologist-Microbiologist, Professor of Microbiology, Aristotle University Thessaloniki, Dr. Polychronopoulou Sofia, Coordinating Director Department of Pediatric Hematology-Oncology Agia Sofia Children’s Hospital Athens.

[homeo-care-clinic]

G6PD Deficiency

Glucose-6-phosphate-dehydrogenase, commonly called G6PD is an enzyme that is essential for the normal functioning of red blood cells and plays an important role in the oxidization process to maintain the physiology of our body.

G6PD deficiency is genetic and it is characterized by the X- linked metabolic disorder. The deficiency is followed by a premature breakdown of red blood cells, that is the rate of haematogenesis is less than hemolysis. Due to the rapid destruction of RBCs, hemoglobin found in RBCs fails to carry the oxygen from the lungs to different organs of the body resulting in hemolytic  Anemia.

Cause of G6PD Deficiency

G6PD deficiency is caused by hereditary factors only, no external stimuli contribute to its deficiency.

Symptoms G6PD Deficiency

In the majority of cases, a person does not show any symptoms and remains a carrier of G6PD deficiency for a prolonged time unless he is exposed to certain food or drugs like fava beans, sulpha drugs, or any noxious agent. Generally, symptoms appear when there is the rapid destruction of RBCs, in such situation patient shows the symptoms of hemolytic anemia like the appearance of pale skin, shortness of breath, abdominal pain with backache, splenomegaly, dark urine, tachycardia, headache with dizziness.

Infants with G6PD deficiency show signs of jaundice 1-4 days after birth due to rapid destruction of RBCs, though mild jaundice is a physiological phenomenon noted in newborns, but the prolongation of complaint may suggest G6PD deficiency.

Nutritional Management :

Though G6PD deficiency is genetically caused, there are some supportive nutritional measures to combat the ill effects of hemolytic anemia, these are:

Avoid eating fava beans which can lead to hemolytic anemia.

Avoid using high doses of ascorbic acid supplementation as it leads to hemolysis.

avoid consuming soya products.

Any edible items containing menthol should be avoided.

Increase consumption of food rich in antioxidants like tomatoes, apples, oranges, etc.

Promote the consumption of whole grains like oats, millet, and barley to get an adequate amount of carbohydrates.

A diet rich in vitamins and folic acid should be consumed rather than taking additional supplements.

Excessive amounts of vitamin K supplements have been proven to cause hemolytic anemia.

Scope of homeopathy :

Homeopathy has a significant effect on genetic diseases like G6PD deficiency. The holistic approach of homeopathy helps in the reversibility of disease conditions and the restoration of health back to its normal state. Homeopathic medicines do not have a direct action on a particular part or organ but it acts on the altered immunity and allow the body to heal itself without causing any side effects.

The single remedy thus selected after taking the totality of symptoms into consideration, arrest the progress of premature hemolysis caused by G6PD deficiency and boost the hemoglobin to carry the oxygen from the lungs to another part of the body, thereby promoting the process of oxidization and prevent the complications caused by hemolysis.

There are many homeopathic medicines that act well in hemolytic anemia caused by G6PD deficiency. Some of them are as follows :

Ferrum met: This remedy is indicated when the person has a great weakness. There is paleness of whole skin with pseudo flushes on slight excitement. Headache is pulsating in character with vertigo and ringing in the ears. Shortness of breath with tachycardia is predominantly present.

Aletris farinosa: This remedy acts well when there is extreme weakness and tired feeling throughout the day with a pale face. The patient feels complete loss of energy and powerlessness. Frequent episodes of giddiness and faintness are present.

Ferrum Phos: This remedy can be easily used for people of all age groups. The patient presents with complaints of paleness, and generalized weakness with nocturnal perspiration. There is tachycardia with an increased pulse rate.

Natrum mur: This remedy is useful when hemolytic anemia is associated with weight loss. The patient appears lean, thin, and malnourished with a loss of vital energy. Hemolysis cause a bursting type of headache with nausea and vomiting.

Calcarea Phos: This remedy is indicated when there is anemia with a slow recovery. There is a tendency to develop bone-related issues. A patient has brittle bones, weakness and difficulty in concentration.

Conclusion

In conclusion, Homeo Care Clinic offers a holistic approach to treating G6PD deficiency. The remedies mentioned above can treat the underlying causes of the condition and offer relief from the discomfort. However, it is important to consult a qualified homeopathic practitioner for the correct dosage and duration of treatment. Homeo Care Clinic provides comprehensive care for various ailments, including G6PD deficiency, and offers customized treatment plans based on individual requirements.

To schedule an appointment or learn more about our services, please visit our website or give us a call. Our friendly staff will be happy to assist you.

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[hyenaswine]

oh i forgot to worry about the splenomegaly. glad i remembered

[kaizenhospitals]

What are 3 diseases that affect the spleen?

Splenomegaly, characterized by an enlarged spleen, can stem from diverse causes like infections (such as mononucleosis or malaria), liver ailments (like cirrhosis), blood disorders (like sickle cell anaemia), or specific cancers. Symptoms might not always manifest, but when severe, they can include abdominal pain, early satiety, or increased susceptibility to bleeding. 

[schlauemaus]

Immunmediierte hämolytische Anämie (Hd)

= häufigste hämolytische Anämie

-> es werden Antikörper gegen die eigenen Erythrozyten gebildet

Ursache

primäre/ idiopathische Form: Ursache unbekannt, gegen unveränderte Erys, Diagnose mittels Ausschlussverfahren

sekundäre Form: Ursache für Antikörperbildung ist bekannt (Infektionen, Neoplasien, Medikamente, Impfungen (bis zu ein Monat später), Bluttransfusion, systemischer Lupus erythematodes); in einem Drittel d. Fälle mit immunbedingter Thrombopenie (=Evanssyndrom)

Symptome

je nach Antikörperklasse u. Schweregrad

blasse Schleimhäute, Schwäche (wg. Anämie)

Anorexie

Ikterus

Erbrechen, Durchfall, Fieber

Splenomegalie

Laboruntersuchungen

Blutuntersuchung

-> mgr.-hgr. Anämie, ggr.-hgr. regenerativ (nicht-regenerativ wenn: gerade in Akutphase, Antikörper richten sich nur gegen Ery.-Vorläufer, Entzündung -> Erythropoese vermindert) -> Ery.-Agglutination (=Verklumpung), makro-/ mikroskopisch -> viele Sphärozyten (= kugelige Erys, entstehen bei Hämolyse) -> positiver Coombstest (=direkter Antiglobulintest) -> hohe Akute-Phase-Proteine (c-CRP) -> Oft: Leukozytose -> Hyperbilirubinämie

Harnuntersuchung

Bilirubinurie selten: Hämoglobinurie (bei intravaskulärer Hämolyse)

Diagnose

Anamnese: Impfung? Auslandsaufenthalt? Medis?

Befunde: pos. Coombstest + Autoagglutination + Sphärozyten

Abklärung von Grundursachen: HarnUS (auch bak./vir.), Blutausstriche (Babesien), Serologie/ PCR (Leishmanien, Leptospirose), Röntgen/ Ultraschall (Neoplasie)

Therapie

Behandlung d. Grunderkrankung

Bluttransfusion -> wg. Anämie

Infusion -> Rehydrieren -> Verhindern v. DIC od. Thromboembolie (schwerste Komplikationen)

Glukokortikoid (Prednisolon) -> immunsuppresiv Gabe mit Protonenpumpenhemmern (Omeprazol) + Antaziden (Sucralfat) -> Vorbeugung gastrointestinaler Symptome

Antibiotika -> wenn pathogenbedingt

ev. Thromboembolieprophylaxe (Acetylsalicylsäure + Clopidogrel)

regelmäßige Blutkontrollen, kann bis 3 Wo. dauern bis sich d. Hämatokrit stabilisiert

-> wenn Anämie auf Therapie anspricht

nach 6 Monaten langsames Ausschleichen d. Prednisolons (alle 2 Wo. etwa 1/4tel), regelmäßige Kontrollen (Blut + mikrobiolog. HarnUS)

-> wenn Anämie NICHT auf Therapie anspricht

zusätzliche Gabe v. Zytostatika (Ciclosporin, MMF, Azathioprin), erfordern Kontrolle v. Neutros u. Thrombos alle 1-2 Wo. ev. Splenektomie (umstritten -> Hochrisiko Anästhesie)

-> wenn rezidivierend

lebenslange Prednisolongabe

Prognose

Rezidivneigung recht hoch

ungünstig:

Autoagglutination

intravaskuläre Hämolyse (also mit Hämoglobinurie)

konstant niedrige Retikulozytenzahlen

Leukozytose

Linksverschiebung

Thrombozytopenie

Bilirubin u. Harnstoff hoch im Serum

hohe Leberenzyme

Hypoalbuminämie

[ourhealthcare7]

Why Patients Choose the Best Spleen Surgery in Delhi: Top Surgeons and Advanced Care

Spleen surgery, known as a splenectomy, is a procedure to remove the spleen, an organ located in the upper left part of the abdomen. The spleen plays a vital role in filtering blood, fighting infections, and maintaining overall immune health. However, conditions like spleen enlargement, trauma, or certain blood disorders may necessitate its removal.

Why is Spleen Surgery Performed?Common reasons for spleen surgery include:

Trauma: Injuries to the spleen from accidents or falls can lead to life-threatening internal bleeding.

Blood Disorders: Conditions like sickle cell anemia, thalassemia, or immune thrombocytopenia (ITP) can affect spleen function, making surgery necessary.

Cysts or Tumors: Growths within the spleen that are malignant or cause pain and discomfort may require removal.

Enlargement (Splenomegaly): Infections or diseases can cause the spleen to become abnormally large, putting pressure on nearby organs.

Types of Spleen Surgery

Open Splenectomy: A traditional approach where a surgeon makes a larger incision to remove the spleen.

Laparoscopic Splenectomy: A minimally invasive surgery that uses small incisions and a camera, offering quicker recovery and less pain.

Why Choose Delhi for Spleen Surgery?Delhi is home to some of the best hospitals and surgeons in India, known for their advanced facilities and expertise. Patients prefer Delhi because:

Top Surgeons: Delhi boasts highly skilled, board-certified surgeons with years of experience in spleen surgeries.

Cutting-Edge Technology: Many hospitals in Delhi offer the latest techniques, including laparoscopic and robotic surgeries, which improve outcomes and speed up recovery.

Comprehensive Care: Hospitals in Delhi provide excellent post-operative care, including monitoring for infections and support for a smooth recovery.

Recovery and AftercareAfter spleen surgery, patients need to be vigilant about infections since the spleen plays a crucial role in immune defense. Vaccinations and regular check-ups are often recommended to prevent complications.

[drumangkhanna]

तिल्ली का बढ़ना || Splenomegaly || Natural homeopathic remedies with symptoms || Dr Umang Khanna

https://youtu.be/zKpSutN5o8I