#hepatic hydrothorax

[dranirudh-1234]

What Is Cirrhosis?

Our livers are capable of self-healing and regeneration. However, as scar tissue eventually forms, it loses some of its ability to perform as intended. Circulatory flow to the liver reduces as the number of scars rises. The liver's fundamental functions are also impaired. This may occasionally result in liver failure and even death. Cirrhosis claims more than a million lives annually throughout the world.

In addition to managing difficult liver surgeries, Dr. Aniruddha Bhosale Head of Liver Transplant and HPB Surgery  at His Hospital in Pune, has decades of experience treating liver cirrhosis as well. He is renowned for offering the best Liver cirrhosis treatment in Pune. due to his extensive training and experience.

Let's learn more about cirrhosis today, including its diagnosis and treatment.

Cirrhosis of the liver is a disorder brought on by persistent liver injury. The liver becomes hard and nodular in this syndrome. Fibrosis replaces the liver tissue. When cirrhosis develops, liver damage is permanent. The cirrhotic liver can no longer regenerate.

Cirrhosis classification

1. Compensated Cirrhosis

It is simply a liver that has been damaged yet is still largely functional.

2. Defamed Cirrhosis

The beginning of the signs and symptoms of liver dysfunction is represented by the advanced stage of cirrhosis.

Why may cirrhosis be harmful?

Cirrhosis causes a number of complications, including

Ascites (abdominal fluid)

Edoema (limb fluid)

(Vomiting blood) Variceal bleeding

The encephalopathy of confusion

Hepatorenal Syndrome, or malfunction of the kidneys

Lung condition (Hepatopulmonary syndrome, Hepatic hydrothorax)

liver tumour

The signs of cirrhosis

The symptoms of liver disease that progresses from early fibrosis to cirrhosis typically take years to appear. Early on, there are frequently few, if any, symptoms.

When symptoms appear, they are occasionally misdiagnosed, disregarded, or linked to additional potential causes. However, if the condition worsens, the symptoms could become more obvious. These signs consist of:

Fatigue Confusion

Weakness

Itching

reduced appetite

Loss of weight

Nausea

Simple bruising

Jaundice

ankle, foot, and leg swelling

Bloating due to ascites in the abdomen

Cirrhosis causes

Cirrhosis is most frequently brought on by:

1. Alcohol-related liver disease: This condition is often brought on by   years of heavy drinking.

2.Hepatitis B is a common contributor to cirrhosis.

3.Hepatitis C is the main predictor of liver transplants and one of the    common causes of cirrhosis.

4.Non-alcoholic fatty liver disease: Cirrhosis is more common in people who have diabetes, high blood pressure, obesity, and high cholesterol. With the prevalence of lifestyle disorders rising in our community, this is fast becoming one of the most common causes of liver cirrhosis.

Among the uncommon causes of cirrhosis are:

First Sclerosing Cholangitis

Wilson's disease and other hereditary illnesses

Hepatitis auto-immune

Hemochromatosis

Celiac illness

Medication

Cirrhosis diagnosis

1: liver biopsy

It is the most precise method for determining the stage of cirrhosis. Nowadays, liver biopsies to diagnosis cirrhosis are rarely performed due to advances in radiological techniques.

2. Magnetic resonance elastography or an ultrasound

These methods for detecting cirrhosis are non-invasive.

3. Blood examinations and imaging devices (CT and MRI)

These can be used to track the development of diseases.

Cirrhosis of the Liver Treatment

In Pune, cirrhosis is frequently treatable before it worsens and a liver transplant is necessary.

The cause and severity of the disease play a major role in cirrhosis therapy.

But after diagnosis, treatment should start right away.

The only known treatment for cirrhosis is liver transplantation.

To slow the growth of liver scarring, you should follow the steps listed below, which include:

Avoid consuming alcohol and drugs that can harm the liver.

Avoid over-the-counter herbal supplements and medications because some of them have been linked to liver damage.

The risk of liver damage from prescription drugs is increased by cirrhosis. As a result, the effects on the liver of every prescription should be carefully considered.

Avoid eating raw shellfish that might have bacteria in it. In those with advanced liver disease, it can potentially result in a serious infection.

Exams and hepatitis A and B vaccinations

antiviral medication for treating hepatitis B and C.

Detection and treatment of bile duct obstructions caused by ursodiol, one of the secondary causes of cirrhosis.

Regarding the treatment of people with cirrhosis, nutrition is crucial.

As soon as you receive a cirrhosis diagnosis, you should start treatment. To get the finest care after the diagnosis, you should always speak with a skilled and experienced liver specialist in Pune.

[mcatmemoranda]

Reviewing questions:

Mesothelial cells are cells that line body cavities (including the peritoneum and pericardium, not just the pleura).

Mesothelial cells form a monolayer of specialised pavement-like cells that line the body's serous cavities and internal organs. The primary function of this layer, termed the mesothelium, is to provide a slippery, non-adhesive and protective surface. However, mesothelial cells play other pivotal roles involving transport of fluid and cells across the serosal cavities, antigen presentation, inflammation and tissue repair, coagulation and fibrinolysis and tumour cell adhesion. Injury to the mesothelium triggers events leading to the migration of mesothelial cells from the edge of the lesion towards the wound centre and desquamation of cells into the serosal fluid which attach and incorporate into the regenerating mesothelium. If healing is impaired, fibrous serosal adhesions form between organs and the body wall which impede vital intrathoracic and abdominal movement. Neoplastic transformation of mesothelial cells gives rise to malignant mesothelioma, an aggressive tumour predominantly of the pleura. Although closely associated with exposure to asbestos, recent studies have implicated other factors including simian virus 40 (SV40) in its pathogenesis.

Anyway, mesothelioma is cancer of the pleura associated with asbestos exposure. It can present with dyspnea, chest pain, cough, and hemorrhagic pleural effusion. If you look at the histology, there will be tumor cells with long microvilli and tonofilaments. CT scan will show pleural plaques.

CREST syndrome = Calcinosis, Raynaud phenomenon (vasospasm of fingers in response to cold), Esophageal dysmotility, Sclerodactyly (localized thickening and tightness of the skin of the fingers or toes), Telangiectasias (small dilated blood vessels that can occur near the surface of the skin or mucous membranes; spider veins). CREST syndrome is the limited cutaneous form of systemic sclerosis. Sysemic sclerosis can lead to pulmonary arterial hypertension due to remodeling of pulmonary arteries and arterioles. Activated T cells secrete TGF-beta, which causes fibroblast proliferation-> excess collagen deposition. There is also excess endothelin (vasoconstrictive) and TXA2 (enhances proliferation)-> vasoconstriction.

I didn't know fluid could go through the diaphragm. There are fenestrations in the diaphragm through which fluid from ascites can travel, causing pleural effusion. Specifically, the ascites in a pt with cirrhosis can cause hepatic hydrothorax, which is a transudative pleural effusion. The pleural effusion is usually on the right side. I don't think I've ever heard of hepatic hydrothorax.

Endothelin causes vasoconstriction. Thromboxane A2 (TXA2) causes proliferation of vascular smooth muscle. Nitric oxide causes vasodilation. Prostacyclin prevents proliferation of vascular smooth muscle. In Pulmonary Arterial Hypertension (PAH), there's increased endothelin and TXA2 and decreased NO and prostacyclin. This causes constriction of the pulmonary arterioles and arteries and proliferation of the vascular smooth muscle, which causes intimal thickening and thus a decreased lumen of the arterioles/arteries-> increased resistance-> loud P2 (pulmonic component of the S2 heart sound) due to increased pressure in the pulmonary artery, so when the valve closes, it closes forcefully. Endothelin comes from the endothelial cells, binds to the endothelin-1 receptor on vascular smooth muscle cells, and leads to vasoconstriction and proliferation of vascular smooth muscle cells. Endothelin-1 receptor antagonists (e.g. bosentan) prevent this. NO comes from L-arginine in the endothelium, enters vascular smooth muscle cells, increases cGMP-> vasodilation and decreased proliferation of vascular smooth muscle cells. Phosphodiesterase inhibitors (e.g. sildenafil) and nitrates (nitroglycerin) also work the same way (i.e., they increase cGMP-> vasodilation). Arachidonic acid from the endothelium becomes prostacyclin (aka prostaglandin I2), which increases cAMP in the vascular smooth muscle cells-> vasodilation and decreased proliferation of vascular smooth muscle cells. Prostacyclin analogs (epoprostanol) work the same way.

CHF-> pleural effusion because there's more blood in the heart, which isn't pumping well-> increased hydrostatic pressure in the pulmonary vasculature. Glucose in the pleural fluid will be decreased in pts with exudative pleural effusions. WBCs metabolize glucose; more inflammation means more WBCs and thus more glucose is being used up by the WBCs, so the glucose in the pleural fluid will be low. In transudative pleural effusions, there is no inflammation, so the glucose of the pleural fluid will be normal or high. The nucleated cell count of the pleural fluid will be low in a transudative pleural effusion (I'm assuming that's because there aren't a bunch of WBCs in the pleural fluid if it's transudative as compared to exudative, which would have more WBCs [nucleated cells] in the pleural fluid).

Carotid body chemoreceptors transmit information via the glossopharyngeal nerve (CN IX) to the medulla. Aortic arch baroreceptors and aortic body chemoreceptors transmit information via the vagus nerve (CN X) to the medulla. I need to think of a way to remember this: carotid body->CN IX-> medulla and aortic arch-> CN X-> medulla. I thought of a mnemonic: a perfect 10 (X) is like an A, so Aortic chemoreceptors transmit through CN X.

In normal pts, PaCO2 increases trigger increased respiratory rate. In COPD, the respiratory drive is driven by PaO2 instead of PCO2 because chronic retention of CO2 blunts the normal respiratory drive, which is driven by PaCO2. So I guess basically, if you always have high PaCO2, then the chemoreceptors don't pay as much attention to CO2; instead, they rely on low PO2 to cause enhanced respiration. Low O2 (hypoxemia) increases respiratory rate in pts with COPD. This is why giving too much O2 in these pts actually decreases their respiratory drive--you made it so there's high O2 instead of their normal baseline low O2. If the chemoreceptors sense high O2, then they think they don't have to trigger respiratory drive anymore, so the pt will breathe less and actually start retaining even more CO2 than normal. Peripheral chemoreceptors sense PaO2. The carotid and aortic bodies sense PaO2; they respond to low levels of O2 in blood. So if you increase O2 by giving supplemental O2, you prevent those peripheral chemoreceptors from responding. So ironically, COPD pts get oxygen-induced hypercapnia after you give them oxygen--they have high PCO2 if you give them roo much oxygen. But that's not the main mechanism that causes oxgen-induced hypercapnea in these pts--what mostly causes increased PCO2 after O2 administration in these pts is the fact that you've undone the hypoxic vasoconstriction when you give too much O2, therefore blood starts going to less-well ventilated alveoli, so you essentially increased their dead space. This means more blood is flowing to areas without ventilation, so they can't get rid of as much CO2 as they normally can-> hypercapnea.

In the anesthesia meeting this morning, they were talking about a pt who had high PCO2 (65+ mmHg) and who was thus kept intubated after surgery. When they looked at his bicarbonate, they saw that it was high (30 mEq/L) at baseline. That means his body is compensating for long-term CO2 retention. So he normally probably has a high PCO2 and thus his PCO2 (while it would be considered high for a normal person) was probably not high for him specifically. So he probably didn't need to be kept intubated. He already lives at a high PCO2. It's like what I learned in my last rotation about OHS/sleep apnea.

So oxygen doesn't normally regulate respiratory drive, CO2 does. Only when PO2 is less than ~65 mmHg do the peripheral chemoreceptors start responding to oxygen as their stimulus for regulating respiration. In pts with COPD, their chemoreceptors stop responding to PCO2. COPD pts can also be hypoxemic with PO2 less than 65 mmHg. So their chemoreceptors start relying on low PO2 to increase respiratory drive. The peripheral chemoreceptors in the carotid and aortic bodies respond to low PO2 to cause increased respiratory drive. Ironically, giving more O2 in pts with COPD causes even more CO2 retention than normal because the increased oxygen level decreases their respiratory drive. So they get O2 and they start breathing less. But apparently, that's not the major mechanism of oxygen-induced hypercapnia. The major mechanism of oxygen-induced hypercapnia is increased V/Q mismatch. If you give too much O2, the poorly ventilated areas vasodilate, leading to more blood flowing to areas that are not well-ventilated. That's what this question explanation says, but I'm confused. I'm not getting what causes the vasodilation. I guess giving O2 makes the less well ventilated areas better ventilated, but they are still not as well ventilated as the areas that at baseline were already better ventilated. So now blood is going away from the alveoli that were already better ventilated to areas that aren't as well ventilated even after you gave O2. It says this causes increased physiologic dead space, so increased V/Q mismatch.

[whatshouldwecallpccm]

On thoracentesis

When my thoracentesis for an untapped simple hepatic hydrothorax ends up drawing frank blood, my initial reaction is

But then the hgb is < 50 %, I be like

[radiologistrabeea]

The following mechanisms may play a role in the formation of pleural effusion: Altered permeability of the pleural membranes (eg, inflammation, malignancy, pulmonary embolism) Reduction in intravascular oncotic pressure (eg, hypoalbuminemia due to nephrotic syndrome or cirrhosis) Increased capillary permeability or vascular disruption (eg, trauma, malignancy, inflammation, infection, pulmonary infarction, drug hypersensitivity, uremia, pancreatitis) Increased capillary hydrostatic pressure in the systemic and/or pulmonary circulation (eg, congestive heart failure, superior vena cava syndrome) Reduction of pressure in the pleural space (ie, due to an inability of the lung to fully expand during inspiration); this is known as "trapped lung" (eg, extensive atelectasis due to an obstructed bronchus or contraction from fibrosis leading to restrictive pulmonary physiology) Decreased lymphatic drainage or complete lymphatic vessel blockage, including thoracic duct obstruction or rupture (eg, malignancy, trauma) Increased peritoneal fluid with microperforated extravasation across the diaphragm via lymphatics or microstructural diaphragmatic defects (eg, hepatic hydrothorax, cirrhosis, peritoneal dialysis) Movement of fluid from pulmonary edema across the visceral pleura Persistent increase in pleural fluid oncotic pressure from an existing pleural effusion, causing further fluid accumula 🥀🌹🥀🌹🥀🌹🥀🌹 ☢ #radiology #technologist #medicalstudent #imaging #ultrasound #CT #US #MRI #xray #nursingschool #nursingstudent #radiologiaporamor #radiologia #loveradio #radiographer #nurse #nursing #technology #medstudent #medschool #medicalschool #futuredoctors #medicine #medicina #surgery #education #teaching #teachersofinstagram #learning #xraytech ☢ https://www.instagram.com/p/B56BqxmB7hT/?igshid=rsgpvl5v1wkc

[a-young-doctors-journey]

I had the hepatic hydrothorax the other day and was like whaaaaaa. But now we better not forget it.

Well, it didn't take long for IM questions on UWorld to kick my ass

[emmajackielee]

Stuff I Learned: 2010 Medicine MCQ Past Paper

Indications for surgery in infective endocarditis

Failure of antibiotic therapy

Heart failure

Abscess

Vegetation and embolic risk

Mycobacterium avium intracellulare first line

Macrolides

Rifampcin

Ethambutol

Anterior uveitis is associated with all PAIR

Indications for TIPS

Variceal bleeding treatment and prevention

Refractory ascites

Hepatic hydrothorax

Budd-Chiari syndrome

G-CSF indications

Before HSCT in donor

Post-chemo neutropenia (ANC < 1)

Drug-induced agranulocytosis (e.g. clozapine, carbimazole, carbamazepine, cotrimoxazole)

Neutropenic fever

ANC

≤ 0.5 or

≤ 1.0 anticipated to drop down to 0.5 in 24-48 hours

Fever

> 38.3 or

> 38.0 for more than 1 hour

Hydroxychloroquine exacerbates psoriasis

XLA vs. CVID

Influenza vaccination can reduce influenza complications

Absence of sensory loss if characteristic of myasthenia gravis

Hyperaldosteronism is associated with alkalosis

Acidosis increases ionized calcium

PTH is low if hypercalcemia is due to excess vitamin D synthesis

SBP diagnosis

Ascitic fluid WCC > 500/mm^3

Ascitic fluid neutrophil > 250/mm^3

[medicalconsultation-blog]

New Post has been published on Health is priceless. Trust the best.

New Post has been published on http://bit.ly/2EBjGD0

Pneumothorax ex-vacuo or “trapped lung” in the setting of hepatic hydrothorax bmc pulmonary medicine full text

[americanjournalradiology-blog]

Transjugular Intrahepatic Portosystemic Shunt

Transjugular Intrahepatic Portosystemic Shunt (TIPS) is a tract created within the liver using x-ray guidance to connect two veins within the liver. The shunt is kept open by the placement of a small, tubular metal device commonly called a stent.

During a TIPS procedure, interventional radiologists use image guidance to make a tunnel through the liver to connect the portal vein (the vein that carries blood from the digestive organs to the liver) to one of the hepatic veins (three veins that carry blood away from the liver back to the heart). A stent is then placed in this tunnel to keep the pathway open. 

What are some common uses of the procedure? 

1) Variceal bleeding, bleeding from any of the veins that normally drain the stomach, esophagus, or intestines into the liver.

2) Portal gastropathy, an engorgement of the veins in the wall of the stomach, which can cause severe bleeding.

3) Severe ascites (the accumulation of fluid in the abdomen) and/or hydrothorax (in the chest).

Budd-Chiari syndrome, a blockage in one or more veins that carry blood from the liver back to the heart. 

How should I prepare?

You should report to your doctor all medications that you are taking, including herbal supplements, and if you have any allergies, especially to local anesthetic medications, general anesthesia or to contrast materials containing iodine (sometimes referred to as "dye" or "x-ray dye"). Your physician may advise you to stop taking aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs) or blood thinners for a specified period of time before your procedure. 

Women should always inform their physician and x-ray technologist if there is any possibility that they are pregnant. Many imaging tests are not performed during pregnancy so as not to expose the fetus to radiation. If an x-ray is necessary, precautions will be taken to minimize radiation exposure to the baby. See the Safety page for more information about pregnancy and x-rays. 

How does the procedure work?

A TIPS reroutes blood flow in the liver and reduces abnormally high blood pressure in the veins of the stomach, esophagus, bowel and liver, reducing the risk of bleeding from enlarged veins across the esophagus and stomach. 

A TIPS procedure involves creating a pathway through the liver that connects the portal vein (the vein that carries blood from the digestive organs to the liver) to a hepatic vein (one of three veins that carry blood from the liver to the heart). 

A stent placed inside this pathway keeps it open and allows some of the blood that would ordinarily pass through the liver to bypass the liver entirely, reducing high blood pressure in the portal vein and the associated risk of bleeding from enlarged veins. 

How is the procedure performed?

Image-guided, minimally invasive procedures such as a TIPS are most often performed by a specially trained interventional radiologist in an interventional radiology suite or occasionally in the operating room. Some interventional radiologists prefer performing this procedure while the patient is under general anesthesia, while some prefer conscious sedation for their patient. The advantage of general anesthesia is that the patient will not feel anything. 

You will be positioned on your back. You may be connected to monitors that track your heart rate, blood pressure and pulse during the procedure. This procedure is usually completed in an hour or two but may take up to several hours depending on the complexity of the condition and vascular anatomy. 

To know more on improvements in the field of TIPS or TIPS  related research work visit American Journal of Interventional Radiology website.

[meg2md]

Here are some RANDOM ASS things that I vaguely remember from Step 1 that are appearing in my QBank??

Felty syndrome (LOL)

Amiodarone displaces digoxin???

Ehrlichiosis (.....)

Hepatic hydrothorax?

all of my wut

Well, it didn't take long for IM questions on UWorld to kick my ass