Tirthankar Online: December 2008

December 29, 2008

SUBARACHNOID HEMORRAGE - LABORATORY WORK UPS AND FINDINGS

Subarachnoid hemorrhage (SAH) implies the presence of blood within the subarachnoid space from some pathologic process. The common medical use of the term SAH refers to the nontraumatic types of hemorrhages, usually from rupture of a berry aneurysm or arteriovenous malformation (AVM). The scope of this article is limited to these nontraumatic hemorrhages.

Workup
Complete blood count
Prothrombin time, activated partial thromboplastin time
Blood typing and screening
Blood bank typing is indicated when SAH is identified or a severe bleed is suspected.
Intraoperative transfusions may be required.
Troponin I (cTnI): cTnI measurement is a powerful predictor for the occurrence of pulmonary and cardiac complications, but it does not carry additional prognostic value for clinical outcome in patients with aneurysmal SAH (Schuiling, 2005).
Imaging Studies
The initial study of choice is an urgent CT scan without contrast (see Picture 1).
Sensitivity decreases with time from onset and with older resolution scanners.
In one recent study published by New England Journal of Medicine, good quality CT scanning revealed subarachnoid hemorrhage in 100% of cases within 12 hours of onset and 93% within 24 hours of onset (Suarez, 2006). Other studies traditionally report 90-95% sensitivity within 24 hours of onset of bleeding, 80% at 3 days, and 50% at 1 week.
CT also can detect intracerebral hemorrhage, mass effect, and hydrocephalus.
A falsely negative CT scan can result from severe anemia or small-volume SAH.
Distribution of SAH can provide information about the location of an aneurysm and prognosis.
Intraparenchymal hemorrhage may occur with middle communicating artery and posterior communicating artery aneurysms. Interhemispheric and intraventricular hemorrhages may occur with anterior communicating artery aneurysms.
Outcome is worse for patients with extensive clots in basal cisterns than for those with a thin, diffuse hemorrhage.
Cerebral angiography is performed once the SAH diagnosis is made.
This study assesses the following:
Vascular anatomy
Current bleeding site
Presence of other aneurysms
This study helps plan operative options.
Angiography findings are negative in 10-20% of patients with SAHs.
If negative, some advocate repeating angiography a few weeks later.
Magnetic resonance imaging (MRI) is performed if no lesion is found on angiography.
Its sensitivity in detecting blood is considered equal or inferior to that of CT scan.
The higher cost, lower availability, and longer study time make it less optimal for detecting SAH.
MRI mostly is used to identify possible AVMs that are not visible on angiography.
MRI may miss small symptomatic lesions that have not yet ruptured.
Magnetic resonance angiography (MRA) is less sensitive than angiography in detecting vascular lesions; however, many believe CT angiography and/or MRA one day will play a more central role.
Multidetector computed tomography angiography (MD-CTA) of the intracranial vessels is now a routine examination, and it is becoming fully integrated into the imaging and treatment algorithm of patients presenting with acute subarachnoid hemorrhage in many centers in the United Kingdom and Europe (Goddard, 2005). Digital-subtraction cerebral angiography has been the criterion standard for the detection of cerebral aneurysm, but CT angiography has gained more popularity and is frequently used owing to its noninvasiveness and a sensitivity and specificity comparable to that of cerebral angiography (Jayaraman, 2004).
Other Tests
Electrocardiogram
About 20% of SAH cases have myocardial ischemia from the increased circulation of catecholamines.
Typical results are nonspecific ST-and T-wave changes, prolonged QRS segments, U waves, and increased QT intervals.
ECG changes reflect myocardial ischemia or infarction and should be treated in the usual manner. Suspicion of SAH is a contraindication to thrombolytic and anticoagulant therapy.

Lumbar puncture
Lumbar puncture (LP) is indicated if the patient has possible SAH and negative CT scan findings.
Perform CT scan prior to LP to exclude any significant intracranial mass effect or obvious intracranial bleed.
LP may be negative less than 2 hours after the bleed; LP is most sensitive at 12 hours after symptom onset.
Red blood cells (RBCs) in the cerebrospinal fluid (CSF) remain consistently elevated in 2 sequential tubes or punctures in SAH, whereas the number of RBCs in technically traumatic punctures decrease over time.
Xanthochromia (yellow-to-pink CSF supernatant) usually is seen by 12 hours after the onset of bleeding; ideally this is measured spectrographically, although many laboratories rely on visual inspection.
LP findings were thought to be positive in 5-15% of all SAH presentations that are not evident on the CT scan. This number may be no longer valid with the advent of newer generations of CT scans. A recent small retrospective chart review about patients presenting to the emergency department undergoing fifth generation CT scans and LP showed no patients with positive LP and negative CT scan (Boesiger, 2005).

REFERENCE: http://emedicine.medscape.com/article/794076-overview

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.