capa conference 2015 · mechanisms of edema formation: 2 are usually needed vessel tissue volume...

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CAPA Conference 2015 1 Edward Kersh, MD, FACC Medical Director for Telehealth, SCAH Clinical Professor of Medicine, UCSF Definitions Mechanisms Consequences Causes and Evaluation Treatment Edema is not an emergency, but what’s causing it may be Definitions Edema = Palpable swelling produced by expansion of the interstitial fluid volume Anasarca = When massive and generalized Pitting = Edema that retains for a time the indentation produced by pressure. Brawny = non-pitting with thickening and induration Ascites = edema of the abdominal cavity

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Page 1: CAPA Conference 2015 · Mechanisms of edema formation: 2 are usually needed Vessel Tissue Volume Pressure Osmotic pressure Permeability Lymphatic drainage Blue = forces into tissue

CAPA Conference 2015

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Edward Kersh, MD, FACCMedical Director for Telehealth, SCAHClinical Professor of Medicine, UCSF

DefinitionsMechanismsConsequencesCauses and EvaluationTreatment

Edema is not an emergency,but what’s causing it may be

Definitions

Edema = Palpable swelling produced by expansion ofthe interstitial fluid volume

Anasarca = When massive and generalized

Pitting = Edema that retains for a time the indentationproduced by pressure.

Brawny = non-pitting with thickening and induration

Ascites = edema of the abdominal cavity

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Dropsy (1672)

The Middle English dropesiecame through the Old French hydropsiefrom the Greek hydropswhich in turn came fromthe Greek hydo meaning water.

DescriptorsPitting and Non-pitting

Dependant

Sacral

Periorbital

Scrotal

4+

Myxedema

Lymphedema

Brawny

DefinitionsMechanismsConsequencesEvaluationTreatment

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Ernest StarlingEquation, Law, hormones, peristalsis, distal tubule

Jv= rate of flux

k= membrane permeability constant

Pc= capillary hyrostatic pressure

P= interstitial hydrostatic pressure

πc = capillary oncotic pressure

πi = interstitial oncotic pressure

The Brown Dog, 1907

Mechanisms of edema formation:2 are usually needed

Vessel

Tissue

Volume Pressure

Osmoticpressure

Permeability

Lymphaticdrainage

Blue = forces into tissueRed = forces out

VolumeRenal Failure and Nephrotic syndrome

Heart Failure

Cirrhosis

Pregnancy and pre-menstrual

Na and fluid overload

Drugs – NSAIDS, vasodilators, EPO

Hormones – estrogen, aldosterone, steroids

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Venous Pressure

DVT

CVI – venous incompetance

Venous stenosis (May Turner syndrome)

OSA

Right heart failure with Pulmonary hypertension

Right heart failure without Pulmonary hypertension

Causes of Right Heart failure

LV, valvular and PVOD

Pulmonary VascularDisease

Cor Pulmonale

Pulmonary EmbolicDisease

RV valve disease

RV dysfunction

Pericardial Disease

Diseases that causepulmonary hypertension

Diseases that cause RV dysfunctionwithout pulmonary hypertension

Osmotic Pressure (low albumin)Nephrotic Syndrome

Enteropathy

Cirrhosis

Malnutrition (Kwashiorkor)

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Permeability

Burns

Trauma

Infection

Allergic reactions

ARDS

Diabetes and TZD’s

Reflex Sympathetic dystropy

IL-2

Anticonvulsants – gabapentin, pregabalin

Chemo – docetaxel, cisplatin

Antiparkinson – pramipexole, ropinerole

ERA’s

Lymphatic ObstructionLymph node dissection

Malignancy

Hypothyroidism

Filariasis

CHF – right sided

Thoracic Duct and edema/ascites

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DefinitionsMechanismsConsequencesEvaluationTreatment

Clinical Manifestations of Chronic Venous Disease

Bergan J et al. N Engl J Med 2006;355:488-498

Hemosiderin

Venous ulcerVaricosities

Telangiectasia

Chronic Venous Valve incompetance

Bergan J et al. N Engl J Med 2006;355:488-498

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Chronic Venous Disease creates Chronic Venous Disease

Bergan J et al. N Engl J Med 2006;355:488-498

Consequences:Venous Disease leads to

More Venous Disease withswelling, skin changes, pain, ulcers

and discoloration

DefinitionsMechanismsConsequencesEvaluationTreatment

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Initial Evaluation – 3 questions

Pitting vs Non-pitting?

Localized (unilateral) vs Generalized (bilateral)?

Onset – acute or chronic

HistoryOnset: acute – DVT, ruptured cyst, infection

chronic – CHF, renal, cirrhosis

Change with position – CVI improves with elevation

Unilateral: DVT, CVI, compression

Bilateral: systemic illness

Medications

Medical History: cardiac, renal, thyroid, liver

OSA

Trauma

ExaminationPitting or Brawny

Tenderness

Discoloration

JVD

Signs of liver disease

Signs of Thyroid disease

Signs of malnourishment

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Venous Clinical Severity Score

Raju S, Neglén P. N Engl J Med 2009;360:2319-2327

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LaboratoryCBC

Creatinine and U/A

BNP

Albumin and LFT’s

D-Dimer ?

ImagingVenous ultrasound

Echocardiogram

MRA or CTA – if ultrasound negative

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DVT DIAGNOSIS: Wells Score

Low Wells Score + negative D-dimer 99% negative predictive value

Differential Diagnosis of Chronic Venous InsufficiencyPain, Swelling, Skin changes, Ulcers

Raju S, Neglén P. N Engl J Med 2009;360:2319-2327

Edema + Ascites Think of:

Cirrhosis

Right Heart Failure

Constrictive Pericarditis

Nephrotic Syndrome

Malnutrition

Malignancy

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Pericardial Disease

Pericardium restricts the fillingof the RV in diastole

Ascites > Edema

DefinitionsMechanismsConsequencesCauses and EvaluationTreatment

Treatment: If you know what’scausing it, you will know how totreat it.

Na+ RestrictionDiuretics: which oneCompression : How much?AnticoagulantsExerciseSomething else

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Pitting Edema

CHFDiuretic decreases plasma volume and reabsorbtion

from tissue restores plasma volume.

Elevation and compression can cause pulmonaryedema

Monitor BUN/creatinne ratio and weight

Oral dose is 2x the IV dose

Thoracic Duct Cannula(something else)

Witte et al, Lymph Circulation in CHF, Circulation 36:723, 1969

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CirrhosisDiuretics – loop diuretic and spironolactone preferred

With no edema reabsorbtion of fluid can lag and causehepatorenal syndrome

Peritoneal drainage (something else)

Renal Failure and nephrotic syndrome

Loop diuretics in higher doses

Monitor BUN/creatinine ratio

Dialysis

Phlegmasia Cerulea Dolens

Can producelower limb ischemiawith compartmentsyndrome and venousgangrene

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Recanalization of an Occluded Iliac Vein with Stent Placement(something alse)

Raju S, Neglén P. N Engl J Med 2009;360:2319-2327

DVT – remember Virchow’s Triad

No Diuretics

Compression 10-20mm

Anticoagulation

Virchow’s Triad

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Prevention of Recurrence

Travel advice: seating, walking, anticoagulants

CVI

CVIElevation

Compression (20-30 mild/30-40 severe)

Pneumatic device (only if socks contraindicated)

Exercise

Emollients/steroids

No Diuretics

Be patient

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Exercise:Action of the Musculovenous Pump in Lowering Venous Pressure in the Leg

Bergan J et al. N Engl J Med 2006;355:488-498

Compression garments

• Daily

• Graduated compression

• Distal to proximal pressure

• Greatest pressure is at most distal point

Unna’s Boot

4 x 10 gauze +/- ACE bandage

Zinc Oxide, calamine, acacia,glycerin, castor oil, antibiotics,Steroids

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Brawny Lymphedema

LymphedemaDecongestive physiotherapy

Compression (30-40 mm)

Pneumatic device

Skin care

OSACPAP

Diuretics with right heart failure

PAH therapy

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Overtreatment

Diuretics are useful with increase volume

Rapid removal can cause hypovoemia

Diuretics are harmful with decreased volume

Signs of decreased volume: Hypotension

Tachycardia

Orthostasis, weakness, syncope

Increased BUN/Creatinine ratio

Hemoconcentration

Conclusions:

Everything is not just swell

But, You don’t die from edema

However, You can die from what’s causing it

And, edema can cause significant morbidity

Accurate Diagnosis dictates treatment

But the wrong Treatment can cause harm

Venous disease begets Venous Disease

So, secondary prevention is critical

"Only by way of experiment, can we hope toattain a comprehension of the body and themastery of disease and pain.”

Ernest Starling: 1866 (London) – 1927 (Jamaica)