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1. Approach to a patient with body swelling
Prepared by : Alazar Bogale
Hinsene Legesse
Aziza Jemal
Modulator :Dr.Mulugeta
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2. Objectives
 Review basic underpinnings of edema development
Provide a comprehensive look at the various causes of edema
 Identify key clinical features to “narrow the differential”
 Brief management pearl
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3. Why is Swelling Important?
“Am I going to die”?
 Unattractive, uncomfortable
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4. • Edema - represents an excess of interstitial fluid that has become
evident clinically. Cardiac, renal, hepatic, or nutritional disorders are
responsible for a large majority of patients with generalized edema.
• Generalized edema not clinically apparent until interstitial volume has
increased by 2.5-3 liters
Approximately 60% of lean body weight is water.
 2/3 of total body water = intracellular
 1/3 = extracellular compartments, mostly the interstitium (or
third space) that lies between cells.
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5. …
There are two overriding factors for edema formation:
1. altered capillary hemodynamics.
2. retention of Na and Water by the kidneys
Fluid collections in the different body cavities are variously
designated :Hydrothorax ,Hydropericardium
,Hydroperitoneum (more commonly called ascites).
Anasarca is a severe and generalized edema with
widespread subcutaneous tissue swelling.
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6. Edema types
transudate… heart failure, renal failure, hepatic
failure, and certain forms of malnutrition.
Exudate/inflammatory edema… result of increased
vascular permeability.
Pathophysiologic mechanism of edema include
1. increase hydrostatic pressure
2. reduced plasma oncotic pressure
3. sodium and water retention
4. lymphatic obstrution , eg : parasitic filariasis
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7. …
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8. Pathways leading to systemic edema from primary heart
failure, primary renal failure, or reduced plasma osmotic
pressure (e.g., from malnutrition, diminished hepatic
synthesis, or protein loss from nephrotic syndrome).
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9. Morphology in edema
Edema is easily recognized grossly.
Microscopically… clearing and separation of the extracellular matrix
and subtle cell swelling.
Any organ or tissue can be involved, but edema is most commonly
seen in subcutaneous tissues, the lungs( mostly seen in left ventricular
failure ), and the brain( life threatening because of herniation ).
Is most easily seen in the skin.
Grading of edema
Grade 1 (Mild
edema)
Both feet/ankles
Grade 2 (Moderate
edema)
On both feet & lower legs; hands &
forearms; Pretibial edema
Grade 3 (Severe
edema)
Generalized bilateral pitting edema,
including both feet, legs, arms and face 9
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10. Edema can be classified as pitting and non-pitting.
 Pitting is when, after pressure is applied (for 3-5 Sec) to a small area,
the indentation persists after the release of the pressure. It is caused by
systemic diseases, pregnancy in some women.
Non-pitting edema is when the indentation does not persist. It is
associated with conditions like lymphedema, lipedema, and
myxedema
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11. APPROACH TO PATIENT
Detailed History
Sound physical exam
Basic labs and imaging
Rarely, advanced labs/imaging
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12. Pivotal Points
It’s all in the history!
Abrupt vs gradual
 Unilateral vs bilateral
Painfull vs painless
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13. Timing
Abrupt, Acute swelling (< 72
hours)
 DVT, cellulitis, ruptured
popliteal cyst, acute
compartment syndrome
 Often unilateral
Systemic process
 Begins simultaneously in each
leg and advances to the same
degree in each leg
Upper limb/facial edema
clinches
Duration
Appears dramatically and
disappears completely with
recurrences of
similar pattern
Infectious, recurring injury,
idiopathic/cyclic edema
But not venous insufficiency or
chronic lymphatic obstruction
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14. Pain + Edema?
Painful
 Cellulitis
 DVT
 Baker’s cyst rupture
 Gastroc rupture
Painless
 Lymphedema
 Systemic causes
Usually, more generalized
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15. Laterality
Unilateral
 More possibilities
The two most common are:-
DVT, Lymphedema
Pelvic obstruction
Intrinsic or extrinsic
Retroperitoneal fibrosis
 Fictitious disorder
Look clues of constrictive device
History of underlying psychiatric disease
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16. Bilateral
Usually systemic
No associated precipitating event
If supine, inspite of leg swelling sacral edema is common
Pain unlikely
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17. Common Causes of Bilateral Edema
acute Chronic
Venous insufficience
Pulmonary hypertension
Heart failure
Idiopathic edema
Drugs
Premenstrual edema
Pregnancy
Obesity
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18. Less Common Causes of Bilateral Edema
Active Chronic
Bilateral DVT Renal disease (nephrotic syndrome or
nephritis)
Acute CHF, Renal disease Liver disease
Secondary Lymphedema (tumor, XRT,
infection
Pelvic tumor or lymphoma (extrinsic
compression)
Dependent edema
Diuretic induced
Pre-eclampsia
lipedema
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19. Common causes of unilateral edema
Acute(<72hr) chronic
DVT Chronic venous insuffieciency
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20. Less common causes of unilateral edema
Acute Chronic
Ruptured Baker’s Cyst Secondary Lymphedema
Ruptured Medial Head of the
Gastrocnemius
Extrinsic venous compression (tumor/
lymphoma)
Compartment Syndrome Reflex Sympathetic Dystrophy
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21. Discussion of Common etiologies of edema
1. Chronic Vein Disease
 is a spectrum of disorders characterized by venous dilation and/or
abnormal vein function in the lower extremities resulting from
venous hypertension
Risk factors for chronic venous insufficiency
↑ Age
↑ BMI
Family history of venous disease
Laxity of ligaments (hernias, flat feet)
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22. Prolonged standing
Smoking
Prior DVT
Klippel–Trenaunay syndrome
 (includes congenital
 absence of venous valves)
↑ Estrogen
 states, including pregnancy
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23. Pathophysiology
Venous hypertension
DVT
 (obstruction) and/or primary valve incompetence (reflux) can cause:
↑ Venous pressure in deep veins
↑ Pressure in perforating veins
↑ Pressure in superficial veins
Endothelial dysfunction of vein walls ensues from DVT
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24. Chronic inflammation of vein walls leads to eventual remodeling of
those vein walls:
↑ Type 1 collagen
↓ Type 3 collagen
↓ Smooth muscle cells
Degradation of the extracellular matrix
↑ Proteinases lead to increased permeability.
Severe wall dysfunction increases the risk of DVT due to:
Inability to properly move blood forward (stagnation)
Chronic inflammation/endothelial damage
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25. Skin and soft tissue changes[1,2,7]
The increase in venous hypertension is combined with increased
vessel permeability.
This leads to efflux of blood components into the subcutaneous space:
Fluid → edema→ ↑ pressure in the extremity, which may lead to
● necrosis
●Impaired lymph drainage → further fluid accumulation and
impaired waste removal
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26. RBCs (which break down) → hemosiderin deposits
→ skin pigmentation
Proteinases → cutaneous ulcers
WBCs → cytokine release → subcutaneous fibrosis
 (lipodermatosclerosis) → ↓ capillaries in these areas:
White plaques (atrophie blanche)
↓ Blood flow → poor healing and ischemia/necrosis
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27. Clinical Presentation
Spectrum of chronic venous disease[1-3]
Asymptomatic venous dilation
Mild disease:
• Telangiectasias
• Reticular veins
• Varicose veins
• Mild dependent ankle edema
Severe disease (chronic venous insufficiency):
• Significant edema
• Skin
• changes
• Ulcers
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28. Presenting symptoms
Dependent pitting edema
 Lower extremity pain or discomfort
Numbness or tingling
Pruritis
Visible tortuous veins
Skin changes:
● Brown or blue-gray discoloration of the skin from hemosiderin deposits
● statis dermatitis
● Lipodermatosclerosis
● Atropie blanche
● Ulcer
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29. IX
photoplethysmography (PPG)
Ankle–brachial index:
Other: heart, lung, and
abdominal exams:
Catheter-based
(invasive) venography
Testing on venous leg ulcers
Treatment goal
Reduce discomfort.
Prevent and treat skin
 manifestations.
Heal ulcers.
Improve modifiable risk factors.
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30. 2. Lymphedema
Accumulation of lymphatic fluid, typically in the arms or legs, due to a
blockage or damage to the lymphatic system.
Primary (idiopathic)
 Congenital= present at birth or becomes evident by age 2; if familial
“Milroy” syndrome.
 Lymphedema praecox= presents at age 2-35. F:M ratio 10:1; if
familial “Meige” disease
Most common form of primary lymphedema
Usually unilateral and limited to the foot and calf
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31. Secondary (obstructive)
much more common than primary
Usually, not a mystery
• h/o of previous groin irradiation
• h/o of cancer
• h/o of recurrent infection/travel (Filariasis)
• h/o of surgical manipulation/removal of lymph node
Obesity likely most common cause of secondary lymphedema
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32. Primary lymphedema Secondary lymphedema
Isolated congenital defect (simple congenital
lymphedema)
Tumors
Milroy disease (hereditary lymphedema Surgical procedures that sever lymphatic connections
Postradiation fibrosis
Filariasis
• Postinflammatory thrombosis and scarring
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33. 33
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34. Lymphedema Characteristics
 symptoms include :swelling, a
feeling of heaviness or tightness in
the affected limb, decreased
flexibility, and recurrent infections.
 Painless
“Kaposi-Stemmer” sign unable to
pinch 2nd digit dorsal skin fold
 Dorsal “Hump” sign
Prominent skin creases between
toes and dorsal hump.
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35. Treatment for lymphedema typically involves a combination of
techniques aimed at:
 reducing swelling
 improving lymphatic flow and
managing symptoms;These may include manual lymphatic drainage (a
specialized massage technique), compression therapy (using
compression garments or bandages), exercise, skin care, and lifestyle
modifications. In some cases, surgical interventions may be necessary.
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36. 3. Heart failure
AHA and Heart Failure Society of America (HFSA)
“Complex clinical syndrome that results from any
structural or functional impairment of ventricular filling or
ejection of blood leading to cardinal manifestations of
dyspnea, fatigue, and fluid retention.”
The European Society of Cardiology’s (ESC)
“Typical symptoms (e.g., breathlessness, ankle swelling,
and fatigue) and signs (e.g., elevated jugular venous
pressure, pulmonary crackles, and peripheral edema)
caused by a structural and/or functional cardiac
abnormality, resulting in a reduced cardiac output and/or
elevated intracardiac pressures at rest or during stress.”
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37. Classification
Based on Ejection fraction
HF with preserved EF (HFpEF) >50%
HF with reduced EF (HFrEF)<40%
HF with mid-range ejection fraction 40-49%
Time course of heart failure
asymptomatic LV systolic dysfunction
chronic HF
Chronic stable HF vs Decompensated chronic heart failure
New-onset (‘de novo’) HF
Classification based on severity of symptoms
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38. Causes of Heart
Failure
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39. PATHOPHYSIOLOGY
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40. Approach to a patient with HF
On history ask ,symptoms such as fatigue ,SOB, orthopnea
,nocturnal cough,PND,palpitation ,cardiac asthma,ankle swelling
,weight loss (cardiac cachexia ),chest pain ,GI symptoms ,cerebral
symptoms,
Characterization of patient history
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41. Preciptant factors
Remember with the mnemonics
‘‘HEART FAILES’’
 HTN
Endocarditis (IE)
Arrhythmia (manifest with new
onset palpitation and Irregularly
irregular pulse)
 Recurrent rheumatic fever and
myocarditis
Thyrotoxicosis and pregnancy
 Fever
Anemia
Infarction
 Lung infection (e.g. pneumonia)
 Embolism (PE, DVT)
 Stress (Dietary i.e. Salt intake,
Drug withdrawal, Psychological
stress, physical stress)
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42. Complication of HF
Severe CHF
AKI→ resulting from pre renal azotemia (Cardio-renal syndrome)
 Cardio embolic stroke
 Pulmonary hypertension
Cardiac cirrhosis → which may lead to all complication of cirrhosis
like Hepatic encephalopathy, esophageal varices and others
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43. Cardiac cachexia
Endocarditis and Arrhythmia (atrial Fibrillation)
Anemia of inflammation
Fluid and electrolyte disturbances like Hypocalcemia,
hypomagnesemia, hypokalemia, hyponatremia
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44. Physical examination (pertinent findings)
GA : cardiorespiratory distress
Vital sign :SBP decrease,PP diminished ,HTN
PR; tachycardic , weak and irregular pulse
Temperature : febrile or hypothermia
RR : chayne stoke breathing
HEENT:facial puffiness ,pale conjuctiva and pale buccal mucosa
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45. LGS :Thyroid enlargement → thyrotoxicosis is precipitant factor
RS:Pulmonary crackles (rales or crepitations), Pleural effusions,
Consolidation → if there is pneumonia as precipitant.
Friction rub → Sign of pericarditis .
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46. CVS
Arterial examination:Arterial cording from atherosclerosis → best
appreciated at radial arteries
 Bruit especially over the carotid → rare but high risk for stroke
 Pistol shot over femoral artery → AR
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47. Venous examination :Distended neck vein (engorged and pulsatile) →
suggest RSHF, TR.
Raised JVP → suggest RSHF or biventricular failure.
+ve hepatojugular reflex.
Pericordial examination :Hyper active precordium, Silent precordium,
Precordial bulge, Cardiomegaly and ventricular hypertrophy, Murmur
of MR and TR frequently present in patients with advanced HF.
S3 and S4 sound are also common in advanced HF.
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48. Abdominal examination :Hepatomegaly, Ascites, Jaundice
MSS:Peripheral pitting edema.
IS: Pallor → Anemia , Cyanosis and cold extremities → suggest
decreased CO.
NS: Hemiparesis / hemiplegia 2ry to Cardio embolic stroke
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49. 4.ACUTE KIDNEY INJURY
Is defined by the impairment of kidney filtration and excretory
function over days to weeks,
resulting in the retention of nitrogenous and other waste products
normally cleared by the kidneys
is a clinical diagnosis
Classified into three:-
Prerenal, Intrarenal, Postrenal
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50. Diagnostic Definition of AKI
➢ AKI is diagnosed if any one of the following criteria is fulfilled
☛ ↑ in SCr from the baseline by > 0.3mg/dl, with in 48 hours. Or
☛ ↑ in SCr by 50% form baseline, within one week
☛ A ↓ in urine output to <0.5 ml/kg per h for longer than 6 h
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51. Approach to a patient with AKI
History :Symptoms
Prerenal (most common form)
Thirst, decreased urine output, dizziness (hypovolemia)
Renal/intrinsic
Can be glomerular or tubular in etiology.
 Hematuria, edema and hypertension (nephritic syndrome) indicates
glomerular etiology.
 Hemorrhage/bleeding/, sepsis, drug overdose or
surgery- indicates acute tubular necrosis (ATN)
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52. Postrenal.
 Urgency, frequency, suprapubic pain.
Risk factors.
Prerenal
Volume restriction
Glycosuria causing polyuria, hemorrhage, sweating.
Intrinsic
Glomerular: throat or skin infections
 Tubular/tubulointerestitial: exposure to nephrotoxins,current medications,
recent radiologic examinations
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53. Postrenal
 History of prostatic disease, nephrolithiasis, or pelvic malignancy
Complications
 Uremia
 Hypervolemia and hypovolemia
 Hyponatremia
 Acidosis
 Hyperkalemia
 Cardiac complications
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54. Physical Examination
1 GA → coma (uremic encephalopathy)
2 Vital signs
OHT (orthostatic hypotension) → hypovolemia 2ry to extra cellular
fluid depletion, ANS neuropathy ➢ Tachypnoea → from uremic
acidosis ➢ Tachycardia → extra cellular fluid depletion
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55. Chest
Rales - Goodpasture syndrome
Hemoptysis - Wegener
granulomatosis
Cardiovascular system
Reduced jugular venous pressure
(may be not in CHF?)
Murmurs – Endocarditis;
Pericardial friction rub - Uremic
pericarditis.
Abdomen
Pulsatile mass or bruit Atheroemboli
Epigastric bruit suggests renal
vascular hypertension
Tense abdomen;
may indicate elevated intra-
abdominal pressure that can retard
renal venous return & => AKI.
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56. • Genitourinary
CVAT - Nephrolithiasis,
papillary necrosis, renal artery
thrombosis
Suprapubic tenderness –
obstruction
Integumentary
digital ischemia, butterfly rash
Maculopapular rash - Allergic
interstitial nephritis
Musculoskeletal: - Assessment
for peripheral edema; Limb
ischemia, edema
Nervous system: - confusion, loss
of consciousness
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57. Investigations
NB: AKI is clinical diagnosis
RFT(SCr); Urinalysis
By current definitions the
presence of AKI is defined by
an elevation in the SCr
concentration or reduction in
urine output.
Serum electrolytes (Na+, K+,
BUN)
CBC : Anemia is common in AKI
Radiologic evaluation
Bladder catheterization - to rule
out obstruction
Renal ultrasound - to look for
obstruction
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58. Type Uosm UNa FeNa BUN/Cr
Prerenal >500 <10 <1% >20
Intrinsic <350 >20 >2% <15
Postrenal <350 >40 >4% >15
Classic laboratory findings in AKI
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59. Staging
The RIFLE criteria, ADQI group,
aid in the staging of patients with
AKI:
Risk: 1.5-fold ↑ in SCr, or GFR
decrease by 25%.
Injury: 2-fold ↑ in SCr, or GFR
decreases by 50%.
Failure: 3-fold ↑ in SCr, or GFR
decrease by 75%.
Loss: Complete loss of kidney
function (e.g., need for renal
replacement therapy) for more
than 4 weeks
End-stage renal disease:
Complete loss of kidney function
for more than three months
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60. Management of Acute Kidney Injury
General management
1. Optimization of systemic and renal
hemodynamics through volume
resuscitation and judicious use of
vasopressors
2. Elimination of nephrotoxic agents
(e.g., ACE inhibitors, ARBs,
NSAIDs, aminoglycosides) if
possible
3. Initiation of renal replacement
therapy when indicated
Specific management
1.Electrolyte abnormality
Hyponatremia
Hypercalemia
2.Drug dosing
Careful attention to dosages and
frequency of administration of
drugs, adjustment for degree of
renal failure
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61. 4 CHRONIC KIDNEY DISEASE (CKD)
CKD is defined by the presence of kidney damage or decreased
kidney function for three or more months, irrespective of the cause.
Characterized by:-
abnormal kidney function and
Progressive decline in glomerular filtration rate (GFR).
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62. History: Symptoms
electrolyte, and acid-base disorders
Sodium and Water Homeostasis:
peripheral edema (due to Hypernatremia),
SOB, coughing up blood, sweating.
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63. Potassium Homeostasis:
palpitations, dizziness, fainting (arrhythmia due to hyperkalemia).
Metabolic Acidosis:
 weight loss, muscle weakness
Cardiovascular abnormalities
 Ischemic heart disease/CHF
Chest pain, shortness of breath, orthopnea, PND
Pericarditis (uremic)
chest pain with respiratory accentuation
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64. Hematologic abnormalities
Anemia,Fatigue,lightheadedness,
Causes of Anemia in CKD:
Relative deficiency of erythropoietin - primary
cause
Diminished red blood cell survival.
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65. Neuromuscular abnormalities
in avanced untreated kidney failure
involuntary jerking of hands,myoclonus,seizures,
and coma can be seen.
Gastrointestinal and nutritional abnormalities
urine-like odor on the breath,unpleasant metallic
taste (dysgeusia).
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66. Dermatologic abnormalities
Pruritus is quite common and one of the most vexing manifestations
of the uremic state.
patients become more pigmented in advanced CKD
(deposition of retained pigmented metabolites)
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67. Risk factors
Diabetes mellitus
Hypertension
Kidney diseases
Drugs like:NSAIDS,
cyclooxygenase-2 (COX-2) inhibitors,
antimicrobials,
Chemotherapeutic agents,
Family history of kidney disease
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68. Complications
Hyperkalemia
Pulmonary edema secondary to volume overload Infection
Physical Examination
Vital signs
BP: Hypertension; Pulsus paradoxus in pericardial tamponade
RR: Increased respiratory rate and depth in metabolic acidosis
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69. CVS:
Jugular venous pressure raised in fluid overload or pericardial
tamponade
ABD:
Ascites, Tenderness
IS
Excoriation of pruritus, Brown line‘ pigmentation of nails,Bruising
easily.
MSS
Edema and sensory polyneuropathy
NS:
Change in mental status.
Peripheral neuropathy.
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70. Investigations
Serum electrolyte
Hypernatremiatremia is commonly seen in CKD patients
CBC
Lipid profile
Imaging Studies
Renal ultrasound (most useful imaging study), which
Can Verify the presence of two kidneys,
Determine if they are symmetric,
Provide an estimate of kidney size, and
 Rule out renal masses and
Rule out evidence of obstruction
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71. NEPHROTIC SYNDROME
History:Symptoms
Patients usually present with puffiness of eyelids
or periorbital edema especially in the morning on
awakening followed by edema of face and feet.
Patients with progressive disease present with
ascites and generalized anasarca.
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72. Risk factors
diabetic nephropathy
Drugs e.g. NSAIDs
Complications
Infection e.g.UTI
Renal insufficiency
Tissue breakdown and cellulitis
Hypovolemia
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73. Physical Examination
General appearance
moon facies or puffiness of face, periorbital edema.
Vital signs
Pulse/HR and BP (minority of patients may have HTN)
HEENT:
Eye
Icterus sclera, pale conjunctiva/anemia, cyanosis
LGS
Lymph node enlargement
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74. Chest:
Sign of pleural effusion
CVS: Neck veins for JVP
ABD:
Swelling/ascites/
IS:
Skin for alopecia, rash, xanthomas, jaundice
MSS:
Feet for pitting edema
External genitalia for edema
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75. Investigations
Urinalysis
Nephrotic range proteinuria will be apparent by 3+ or
4+ readings on dipstick.
(A 3+ reading represents 300mg/dL of urinary protein or
more.
Glucosuria points to diabetes
Urine sediment examination
Serum albumin: is classically low in NS, being below its
normal range of 3.5 – 4.5 g/dL
CBC—to detect anemia due to renal failure
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76. 6 Chronic liver disease(cirrhosis)
 Cirrhosis represent a late stage of progressive hepatic fibrosis
characterized by distortion of hepatic architecture and formation of
regenerative nodules.
 in early(reversible stage) treat the underlying cause suffice.
 in advanced stage,the only treatment is liver transplantation.
 cirrhosis resulted in hepatocellular mass which decrease the hepatic
function and reduced blood flow.
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77. etiology and classification
 common causes are
-chronic viral hepatitis(B,C)
-alcohol-associated liver disease
-hemochromatosis
-non alcohol-associated fatty liver disease
less common causes are
-autoimmune,primary and secondary biliary cirrhosis
-medication,Wilson,celiac,primary sclerosing cholangitis....Etc.
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78. CONT...
• classification
1)morphologically
-micronodular
-macronodular
-mixed
• But recently this classification is abandoned because of three main reason
1.relatively non specific with regard to etiology,
2.morphologic appearance will change as a liver disease progress.
3.serologic markers are more today available than morphological appearance
of liver for determining the etiology.
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79. Clinical manifestation
May include non specific symptoms(eg:-anorexia,weight loss
,weakness,fatigue)
Or may present with sign and symptoms of hepatic decompensation
 -jaundice,pruritus,sign of upper GI
bleeding(hematemesis,melena,hematochezia),abdominal distension of
ascites,confusion of hepatic encephalopathy.
diarrhea because of small bowel motility,bacterial overgrowth,bile
acid deficiency.
IN women,chronic anovulation which manifest as amenorrhea or
irregular menstrual bleeding due to variation in hormones.
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80. CONT....
Men's with cirrhosis may present with hypogonadism which manifest
as impotence,infertility,loss of sexual drive and testicular atrophy.
parathyroid enlargement and digital clubbing in alcoholic cirrhosis.
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81. Physical finding
GA:- chronically sick looking,fetor hepaticus.
vital sign:-tachypnea(kusmuals breathing),febrile,BMI may
misinterpreted due to edema.
HEENT:-icteric sclera,pale conjunctiva,epistaxis,xanthalasma in eye
and hand crease.
LGS:-gynecomastia,parathyroid enlargement,testicular atrophy.
Respiratory system:-kusmuauls breathing,cyanosis,clubbing,pleural
effusion.
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82. CONT....
Cardiovascular system:-right side heart failure due cardiac cirrhosis.
Abdominal examination:-hepatosplenomegaly,ascites,caput
medusa,bruit over aorta secondary to HCC,tenderness and rebound
tenderness.
genitourinary examination:-loss of male hair type
distribution,testicular atrophy,amenorrhea.
musculoskeletal examination:-bilateral piting edema,duptyren
contracture.
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83. CONT...
Integumentary examination:-spider angiomas,palmar erythema,palmar
pallor,skin pigmentation,purpura,bruising,leukonychia,axillary and
pubic hair loss.
Nervous system:-asterixis,coma,hyperreflexia.
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84. Major complication
Portal hypertension related
 -ascites
 -gastroesophageal varices
 -hemorrhoid's
 -portal hypertension
Hepatic insufficency realted
 -hepatic encephalopahty
 -hepatopulmonary
 -hepatorenal
 -hematologic abnormalities
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85. Investigation
LFT
LIVER ENZYME TEST
VIRAL MARKERS
ASCITES FLUID ANALYSIS
CBC
PERIPHERAL MORPHOLOGY
SERUM ELECTROLYTE
ABDOMINAL U/S
CXR,ECG,ECHO
SERUM AUTOANTIBODIES
LIVER BIOPSY
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86. Management
prevention
 -vaccination
 -avoidance of hepatotoxins
 -medication adjustment
supportive management like
 -diet,bed rest.
treating the underlying causes
treating the complication
if indicated liver transplantation
close follow up and advising on lifestyle.
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87. In Summary
Edema is common and presents a vast differential to the office
clinician
•Using low tech readily available skills, the diagnosis can usually be
identified
spending a bit of time up front on the H/P pays big dividends on the
back-end
Effective Rx is dependent on accurate diagnosis
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88. References
• Creager, M. A., Loscalzo, J. (2008). Vascular disorders of the extremities. In
Fauci, A. S., Braunwald, E., Kasper, D.L., et al. (Eds.) Harrison’s Internal
Medicine (17th ed., p. 1574).
• Kabnick, L. S., Scovell, S. (2020). Overview of lower extremity chronic
venous disease. In Collins, K. A. (Eds.) UpToDate. Retrieved February 14,
2021, from https://www.uptodate.com/contents/overview-of-lower-
extremity-chronic-venous-disease
• *2_Harrison's_Principles_of_Internal_Medicine,_19E_2016_True_PDF.pdf
• Uptodate 2024
• Robbins Basic Pathology (9th Edition).pdf
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89. THANK YOU
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