Symptom To Diagnosis - Edema Flashcards
GENERALIZED edema due to a systemic cause - General etiologies:
- Cardiovascular.
- Hepatic (cirrhosis).
- Renal.
- Anemia.
- Nutritional deficiency.
- Medications.
- Refeeding edema.
- Myxedema.
Cardiovascular causes of edema:
- Systolic or diastolic dysfunction, or both.
- Constrictive pericarditis.
- Pulmonary HTN.
Medications that cause generalized edema:
- Antidepressants: MAOIs.
- Antihypertensives: CCBs, hydralazine, minoxidil, beta-blockers.
- Hormones: Estrogens/progesterones, testosterone, steroids.
- NSAIDs and COX-2 inhibitors.
Limb edema - General etiologies:
- Venous diseases (obstruction + insufficiency).
- Lymphatic obstruction.
- Localized edema.
Venous disease as a cause of limb edema:
- OBSTRUCTION –> DVT, lymphadenopathy, pelvic mass.
2. INSUFFICIENCY.
Lymphatic obstruction as a cause of limb edema:
- PRIMARY –> (idiopathic, often bilateral), congenital, lymphedema praecox (onset in puberty) or tarda.
- SECONDARY –> (more common generally unilateral), neoplasm, surgery (esp. mastectomy), radiation, miscellaneous (TB, recurrent lymphangitis, filariasis).
Localized edema:
- Burns.
- Angioedema/hives.
- Trauma.
- Cellulitis, erysipelas.
MCC of cirrhosis:
- Alcohol.
- Chronic hep B, C.
- NAFLD.
- Hemochromatosis.
- Primary/secondary biliary cirrhosis.
Less common causes of cirrhosis:
- Drugs and toxins (isoniazid, methotrexate, amiodarone).
- Autoimmune hep.
- Genetic metabolic diseases (Wilson, alpha-1 antitrypsin def., glycogen storage diseases, porphyria).
- Infections (schistosomiasis, echinococcosis, brucellosis).
- Cardiac.
2 MCC of cirrhosis in the USA:
- Alcoholic liver disease.
2. Chronic hep C.
Risk factors for developing cirrhosis in patients with hep C:
- > 50.
- Regular alcohol.
- Male sex.
Risk factors for developing cirrhosis for those with NAFLD:
- Older age.
- Obesity.
- Insulin resistance.
- HTN.
- Hyperlipidemia.
Typical patient with ascites - Problem with daily living?
Patient complains of an inability to fasten her pants due to increasing abdominal girth, sometimes accompanied by dyspnea and edema.
Diagnostic criteria of hepatorenal syndrome:
- Cirrhosis with ascites.
- Serum Cr >1.5.
- Serum Cr stays above 1.5 after at least 2 days of diuretic withdrawal and volume expansion with albumin.
- Absence of shock.
- No current or recent treatment with nephrotoxic drugs.
- Absence of parenchymal kidney disease.
Type I hepatorenal syndrome:
Acute renal failure: Serum creatinine doubles or increases to >2.5 in less than 2 weeks.
Type II hepatorenal syndrome:
Refractory ascites: Serum creatinine 1.25-2.5 with a steady or slowly progressive course.
Hepatorenal syndrome - Incidence in patients with cirrhosis at 1yr and in 5yrs:
18% at 1 yr.
39% at 5 yrs.
Precipitants of type I hepatorenal syndrome:
- Bacterial infections (esp. SBP).
- GI bleeding.
- Alcoholic hep.
- Overdiuresis.
- Large volume paracentesis.
Hepatorenal syndrome - Mechanism:
Peripheral vasodilation –> Decreased systemic vascular resistance –> Renal arteriolar vasoconstriction –> Decreased renal blood flow and a reduced GFR.
SPB - Prevalence:
10-30% of hospitalized cirrhotic patients.
SBP - Recurrence rate in 1yr:
70%.
SBP - Mortality rate of:
20%.
3 common isolates in SBP:
- E.coli.
- Klebsiella.
- Pneumococci.
SBP - Symptoms:
50-75% --> Fever. 27-72% --> Abdominal pain. 16-29% --> Chills. 8-21% --> Nausea/vomiting. Up to 50% --> Mental status changes. 33% --> Decreased renal function.
SBP - Percentage of patients who are asymptomatic:
13%.
Risk factors for SBP:
- Ascitic fluid total protein level <1g/dL.
- Upper GI bleeding.
- Prior episode of SBP.
Criteria for performing a diagnostic paracentesis in patients with cirrhosis and ascites:
- Admission to the hospital.
- Change in clinical status.
- Development of leukocytosis, acidosis, or renal failure.
- Active GI bleeding.
Interpretation of ascitic fluid results - PMN >250 with single organism:
SPB.
Interpretation of ascitic fluid results - PMNs >250 with negative cultures:
Culture-negative neutrophilic ascites.
Interpretation of ascitic fluid results - PMN<250 with single organism:
Monomicrobial non neutrocytic bacterascites.
Interpretation of ascitic fluid - PMN >250 and polymicrobial:
Secondary bacterial peritonitis.
Interpretation of ascitic fluid - PMN<250 and polymicrobial:
Polymicrobial bacterascites.
LR + of SAAG >1.1 for the diagnosis of ascites due to portal HTN:
4.6.
LR- of SAAG<1.1 for the diagnosis of ascites due to portal HTN:
0.06.
Hepatic encephalopathy - Presents in …-…% of patients with chronic liver disease.
50-70%.
Hypersplenism in cirrhosis - Textbook presentation:
Cytopenias are found on routine blood testing in a patient with cirrhosis.
Splenomegaly is found in …-…% of patients with cirrhosis.
…-…% have the clinical syndrome of hypersplenism.
36-92%.
11-55%.
Is there a rough correlation between spleen size and decrease in RBCs?
Yes.
Mechanisms of thrombocytopenia in liver disease:
- Platelet sequestration in the spleen.
- Impaired bone marrow production.
- Decreased platelet survival.
Mechanism of leukopenia in liver disease:
Sequestration in spleen - RARE compared to thrombocytopenia.
Mechanism of anemia in liver disease:
- Increased destruction in spleen.
- Iron or folate deficiency.
- Decreased EPO production.
Nephrotic syndrome - Textbook presentation:
- Edema.
- HTN.
- Hypoalbuminemia.
- Hyperlipidemia.
at least 3.5g/24h of proteinuria.
Infections that lead to nephrotic syndrome:
- Hep B,C, HIV.
- Syphilis.
- Malaria.
Malignancies associated with nephrotic syndrome:
- Lung.
- Breast.
- Colon.
- HL.
3 drugs that may cause nephrotic syndrome:
- NSAIDs.
- Captopril.
- Heroin.
Risk factors for thromboembolism in nephrotic syndrome:
- Serum albumin 8g/24h.
Lab evaluation of nephrotic syndrome:
- CBC.
- Comprehensive metabolic panel (renal and liver function, including serum albumin).
- Fasting glucose and HbA1c.
- ANA.
- HIV, hep B, C.
- Serum and urine electrophoresis.
Normal pulmonary arterial pressure is:
12mmHg.
Pulmonary HTN is defined?
As a mean PAP>25mmHg, with a mean pulmonary arterial occlusion pressure Mean PAP of at least 50mmHg.
3 components of the pathophysiology of pulmonary HTN:
- Vascular remodeling with vascular inflammation and endothelial cell proliferation.
- Platelet dysfunction and thrombosis.
- Vasoconstriction due to 2 factors.
Why vasoconstriction in pulmonary HTN?
Endothelial dysfunction resulting in:
1. OVERproduction of endothelin-1.
2. UNDERproduction of vasodilators such as NO, PGI2, VIP.
+ ABNORMAL voltage-gated K channels.
Clinical classification of pulm. arterial HTN (PAH):
- Idiopathic.
- Familial.
- PAH associated with:
a. Collagen vascular disease (esp. scleroderma, SLE, mixed connective tissue disease).
b. Congenital pulmonary-systemic shunts.
c. Portal HTN (1-6%).
d. HIV (0.5%).
e. Drugs and toxins.
INITIAL Symptoms of PAH:
60% --> Dyspnea. 19% --> Fatigue. 7% --> Chest pain. 8% --> Syncope. 3% --> Edema.
At the time the patients were given the diagnosis of PAH and were enrolled in the study:
98% --> Dyspnea. 73% --> Fatigue. 47% --> Chest pain. 37% --> Edema. 36% --> Syncope. 33% --> Palpitations.
PAH - Physical exam:
- Accentuated pulm. component of S2.
- Sustained left lower parasternal movement.
- An early systolic click.
- Increased jugular a and v waves.
- TV regurgitation.
- Hepatojugular reflex.
- Pulsatile liver.
- Elevated jugular venous pressure.
- Edema.
Sustained left parasternal movement for detecting a mean PAP>50mmHg:
Sens - 71%.
Spec - 80%.
LR+ 3.6.
LR- 0.4.
A palpable P2 for detecting a mean PAP>50mmHg:
(studied in patients with MV stenosis). Sens - 96%. Spec - 73%. LR+ 3.6. LR- 0.05.
ECG - Expected findings in PAH:
- Right axis deviation.
- RV hypertrophy.
- P-pulmonale pattern.
NOT sensitive or specific enough to diagnose PAH.
Venous insufficiency - Superficial or deep veins of the leg?
45% –> Superficial system.
40% –> Deep system + Superficial system.
Remainder –> Only deep system.
Prevalence of varicose veins:
25-33% –> Women.
10-20% –> Men.
Prevalence of skin changes in venous insufficiency:
3-11% –> Skin changes.
0.3-1% –> Skin ulcers.
Risk factors for venous insufficiency:
- Age.
- Obesity.
- History of phlebitis or venous thrombosis.
- Serious leg trauma.
- Pregnancy.
- Prolonged standing.
- Greater height.
Classification of venous insufficiency:
Class 1: Telangiectasias or reticular veins (non palpable subdermal veins up to 4mm in diameter).
Class 2: Varicose veins. (palpable >4mm in diameter).
Class 3: Edema without skin changes.
Class 4: Skin changes.
Class 5 and 6: Healed or non healed ulcers.
Gold standard for venous insufficiency:
Venography.
Best non invasive test for venous insufficiency:
Duplex US.
Cellulitis definition:
An infection of the dermis and subcutaneous tissue.
Erysipelas definition:
Superficial cellulitis with prominent lymphatic involvement.
Risk factors for the development of cellulitis:
- Lymphedema.
- Peripheral edema.
- Venous insufficiency.
- Obesity.
- Diabetes.
- History of cellulitis.
- Breast cancer treatment.
Cellulitis - Presence of systemic symptoms (fever, chills, myalgias)?
UNUSUAL –> Suggests concomitant bacteremia or a more serious infection such as necrotizing fasciitis.
Risk factors for erysipelas:
- Similar to those for cellulitis.
2. Lymphedema and an identified portal of entry (primarily tinea pedis) are the 2 strongest risk factors in 1 study.
Most common site for erysipelas?
Leg –> 90%.
5% –> Arm.
2.5% –> Face.
BOTH cellulitis and erysipelas are … diagnoses.
Clinical.
Erysipelas/cellulitis - Blood cultures are positive in …-…% of patients.
2-5%.
Erysipelas/cellulitis - Skin biopsy cultures are positive in …-…% of patients.
5-40% - RARELY necessary.
UPPER extremity DVT (UEDVT) - Textbook presentation:
Patients can be asymptomatic, but generally arm, shoulder, or neck discomfort or fullness as well as arm swelling are the presenting symptoms.
Classification of UEDVT:
Primary (20%).
Secondary (80%).
Effort thrombosis?
Paget-Schroetter syndrome:
- Young men after strenuous exercise, which causes microtrauma to the veins.
- May or may not find compression by hypertrophied muscles or a cervical rib.
Secondary UEDVT - Etiology:
- Indwelling central venous catheter-associated UEDVT (up to 70% of cases).
- Malignancy (>40% of cases).
- Hypercoagulable states.
- Other miscellaneous causes (surgery, infection, immobility, concurrent lower DVT).
UEDVT - Sites:
18-69% –> Subclavian.
5-42% –> Axillary.
8-29% –> Internal jugular vein.
4-13% –> Brachial.
UEDVT - Clinical features:
80% –> Edema.
40% –> Pain.
Patients may note numbness, heaviness, paresthesias, pruritus, coldness.
Dilated cutaneous veins sometimes visible.
UEDVT - Complications:
- PE –> 36%.
- Recurrent thrombosis –> 10%.
- Post thrombotic syndrome is seen in up to 4-34% of patients in different sites.
How much must the interstitial volume be increased for edema to be clinically present?
2.5-3L.