Tirthankar Online: Laboratory diagnosis of Generalised Edema (Anasarca)

January 15, 2012

Laboratory diagnosis of Generalised Edema (Anasarca)

Edema is defined as collection of excess fluid in tissue space or serous cavities. Generalised edema is also called Anasarca.

Common causes of anasarca are:

a. Renal disease – Nephrotic syndrome
b. Hepatic disease – Cirrhosis of Liver
c. Cardiac disease – Congestive cardiac failure

Investigations:

Baseline:

a. Complete hemogram
b. Blood Sugar, Urea, Creatinine
c. Chest X ray – PA view
d. ECG in 12 leads

Special:

a. Echocardiography
b. Serum albumin
c. LFTs
d. Prothombin time
e. Urine R/E
f. 24 hour urinary protein excretion
g. Examination of effusion/ ascitic fluid

Complete hemogram

· Hb – may be reduced in chronic renal disease
· RBCs may show macrocytosis or target cells in chronic liver disease

Blood sugar

· To rule out Diabetes Mellitus

Urea/ Creatinine

· May rise in Renal disorder and left Heart failure

Chest X Ray

· May show evidence of pulmonary edema (bat wing appearance of hilar region)
· May show evidence of Pleural and Pericardial effusion (due to hypo-albuminemia)
· May show cardiac hypertrophy in chronic heart diseases

ECG in 12 leads

· Shows patterns of Ventricular hypertrophy
· Gives early evidence of electrolyte disbalance (in renal failure)

Echocardiography

· Confirms heart failure (LV ejection fraction < 55%)
· Detects ventricular hypertrophy
· Detects pericardial effusion

Serum albumin

· Reduced in hepatic disease and nephrotic syndrome
· Unchanged in heart failure

Liver function tests

· Abnormal in cirrhosis (raised AST, ALT, reduced albumin, altered albumin:globulin ratio)

Prothrombin time

· Raised in cirrhosis
· Reduced in nephrotic syndrome
· Unchanged in cardiac failure

Urine Routine Examination

In nephrotic syndrome, following changes are expected:

· Physical – appearance is hazy, high specific gravity
· Chemical – protein +++
· Microscopic – fatty cast +, hyaline cast +++

24 hour urinary protein excretion

· Raised in nephrotic syndrome (often > 3.5 g/day)

Examination of pleural fluid in case of pleural effusion

· State the differences between transudate and exudate (from your textbook/ copy)

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Answers to your questions

2. Short note on SSSS.(Deborshi)

Ans:
Definition:

Staphylococcal scalded skin syndrome (SSSS) is an acute epidermolysis caused by a staphylococcal toxin.

Newborns and children are most susceptible. Symptoms are widespread bullae with epidermal sloughing. Diagnosis is by examination and sometimes biopsy. Treatment is antistaphylococcal antibiotics and local care. Prognosis is excellent with timely treatment.

Staphylococcal scalded skin syndrome (SSSS) almost always affects children < 6 yr (especially infants); it rarely occurs in older patients unless they have renal failure or are immunocompromised. Epidemics may occur in nurseries, presumably transmitted by the hands of personnel in contact with an infected infant or who are nasal carriers of Staphylococcus aureus. Sporadic cases also occur.
SSSS is caused by group II coagulase-positive staphylococci, usually phage type 71, which elaborate exfoliatin (also called epidermolysin), a toxin that splits the upper part of the epidermis just beneath the granular cell layer. The primary infection often begins during the first few days of life in the umbilical stump or diaper area; in older children, the face is the typical site. Toxin produced in these areas enters the circulation and affects the entire skin.

Symptoms and Signs

The initial lesion is usually superficial and crusted. Within 24 h, the surrounding skin becomes painful and scarlet, changes that quickly spread to other areas. The skin may be exquisitely tender and have a wrinkled tissue paper–like consistency. Large, flaccid blisters arise on the erythematous skin and quickly break to produce erosions. Intact blisters extend laterally with gentle pressure (Nikolsky's sign). The epidermis may peel easily, often in large sheets. Widespread desquamation occurs within 36 to 72 h, and patients become very ill with systemic manifestations (eg, malaise, chills, fever). Desquamated areas appear scalded. Loss of the protective skin barrier can lead to sepsis and to fluid and electrolyte imbalance.

Diagnosis

· Biopsy
· Cultures may be useful in adults

Diagnosis is suspected clinically, but confirmation usually requires biopsy (frozen section may give earlier results). Specimens show noninflammatory superficial splitting of the epidermis. In children, skin cultures are seldom positive; in adults, they are frequently positive. Cultures should be taken from the nose, conjunctiva, throat, and nasopharynx.

Differential diagnosis:

Differential diagnosis includes drug hypersensitivity, viral exanthemas, scarlet fever, thermal burns, genetic bullous diseases (eg, some types of epidermolysis bullosa), acquired bullous diseases (eg, pemphigus vulgaris, bullous pemphigoid), and toxic epidermal necrolysis. Stevens-Johnson syndrome is characterized by mucosal involvement, which is absent in SSSS.

Differentiating Staphylococcal Scalded Skin Syndrome (SSSS) and Toxic Epidermal Necrolysis (TEN)

SSSS

i)Patients affected - Infants, young children, immunocompromised adults

ii)Patient history - Recent staphylococcal infection, renal failure

iii) Level of epidermal cleavage (blister formation)* - Within the granular cell (outermost) layer of the epidermis

TEN

i)Patients affected - Older patients

ii)Patient history - Drug use

iii)Level of epidermal cleavage (blister formation)* - Between the epidermis and dermis or at the level of the basal cell

*Determined by Tzanck test or by a frozen section of a fresh specimen.

Treatment

· Antibiotics
· Corticosteroids not recommended
· Gel dressings for weeping lesions

With prompt diagnosis and therapy, death rarely occurs; the stratum corneum is quickly replaced, and healing usually occurs within 5 to 7 days after start of treatment.Penicillinase-resistant antistaphylococcal antibiotics given IV must be started immediately.

1. Comment: carcinoma usually spreads through lymphatics. (Himel)

Answer: It is a common dictum that carcinomas usually spread via lymphatics, and sarcomas usually spread through blood vessels. Most carcinomas metastasise by lymphatics, which include Ca breast, Ca stomach, Ca uterus, etc. However, it is not a universal dictum, as some Ca preferencially spreads via blood vessels, like renal cell carcinoma.

Recent research has thrown light on the probable reason behind this peculiar preference. The tumors that spread via blood vessels produce sufficient local angiogenesis, so that the tumor is well supplied by micro vessels that help in hematogenous spread. However, tumors that metastasise through lymphatics are rarely supplied with micro lymphatics. Instead, they have a surrounding chain of lymphatics outside the tumor mass. The spread into these vessels is facilitated if the surface area of the micro lymphatics can be increased or if the growth of intra-tumor lymphatics can be facilitated.. It is seen that the carcinomas that spread via lymphatics secrete higher amounts of VEGF-C, VEGF-D, VEGF-A and PDGF-BB, the growth factors that increase the number and the surface area of the lymphatics and facilitates the invasion by tumor cells. The higher expression of VEGF gene in carcinomas compared to sarcomas may explain why carcinomas more often spread via lymphatics.