Deep vein thrombosis

The onset of DVT may be silent or heralded by pain in the
calf, often about 10 days after immobilization for
surgery, parturition or an infection. The leg becomes
swollen and cyanotic distal to the thrombus. The calf
may hurt when handled or if the foot is dorsiflexed
(Homans sign). Sometimes a pulmonary embolus is
the first sign of a silent deep vein thrombosis.
Suitable investigations include venography, Doppler
ultrasonography, which can only detect thrombi in
large veins at, or above, the popliteal fossa, and
I-fibrinogen isotope leg scanning.
Treatment is anticoagulation with heparin and
later with a coumarin. The value of thrombolytic
regimens has yet to be assessed properly. Prevention
is important. Deep vein thrombosis after a surgical
operation is less frequent now, with early postoperat-
ive mobilization, regular leg exercises, the use of elastic
stockings over the operative period and prophylaxis
with low dose heparin.

Treatment of Chronic Eczema

This responds best to steroids in an ointment base, but
is also often helped by non-steroid applications such
as ichthammol and zinc cream or paste.
The strength of the steroid is important.
Nothing stronger than 0.5 or 1% hydrocortisone
ointment should be used on the face or in infancy.
Even in adults one should be reluctant to prescribe
more than 200g/week of a mildly potent steroid,
50g/week of a moderately potent or 30g/week of a
potent one for long periods. Very potent topical
steroids should not be used long-term.
Bacterial superinfection may need systemic antibi-
otics but can often be controlled by the incorporation
of antibiotics, e.g. fusidic acid, mupirocin, neomycin
or chlortetracycline, or antiseptics, e.g. Vioform, into
the steroid formulation. Many proprietary mixtures
of this type are available in the UK. Chronic localized
hyperkeratotic eczema of the palms or soles can be
helped by salicylic acid (16% in emulsifying oint-
ment) or stabilized urea preparations.

G6PD Deficiency

G6PD deficiency is an inherited disorder of the red blood cell, inherited in an x-linked
recessive manner – males are affected while the females are carriers. G6PD is an enzyme
essential in keeping glutathione in the reduced state that in turn is vital to maintain the
integrity of the red cell membrane. In G6PD deficiency the red blood cells are prone to
haemolysis when exposed to oxidants or when certain foods or herbs are ingested. A list
of drugs and herbs that can precipitate haemolysis is provided in the appendix (Luzzato,
1992).

The incidence of G6PD deficiency varies among the various ethnic groups as follows -
Chinese 3.1%, Malay 1.4%, and Indian 0.2% (Robinson et al., 1976). These results were
obtained by using a fluorescent screening method, that had been found to be as sensitive
and specific as other screening tests (Fairbanks & Fernandez 1969).

Pathogenesis of Hepatitis B

Eradication of HBV infection depends on the coordinate and efficient development of humoral and cell-mediated immune responses against HBV proteins. Antibodies secreted by plasma cells (PC) derived from antigen-specific B cells (which usually recognize viral antigens in their native conformation) are mostly responsible for the neutralization of free circulating viral particles, Cytotoxic T cells (CTL) that recognize endogenous viral antigens in the form of short peptides associated with human leukocyte antigen (HLA) class I molecules on the surface of the infected hepatocytes (HC) are the main effectors for the elimination of intracellular virus. They can do this by at least two different mechanisms: direct attachment to the cell membrane, causing the infected cell to undergo apoptosis; and the release of soluble cytokines that can downregulate viral gene expression, leading to the elimination of intracellular virus without destruction of the infected cell. Both humoral and cytotoxic functions are more or less stringently regulated by the helper effect of the CD4+ T cells (TH) that recognize exogenous viral antigens, released or secreted by liver cells, in the form of short peptides that associate with HLA class II molecules in the endosomal compartment of professional antigen-presenting cells such as B cells, macrophages (Mø), and dendritic cells.

THE ABC OF STROKE MANAGEMENT

 

ACUTE STROKE

A: Airway

B: Breathing

C: Cardio-respiratory

D: Drugs

E:  Electrolyte

F:  Fluids

G:  Glucose

H:  Hydration

I :  Intake/nutrition : dysphagia à enteral/parenteral nutrition

                                caloric/nutrients/vitamins/trace elements

REHABILITATION: as soon as the condition of patient is stable

 

IMPORTANT THINGS TO BE KEPT IN MIND:

•         STROKE  is first of all a vascular event.It is and should be treated as a part of systemic(vascular) diseases

•         The already infarcted brain tissue can not regenerate.The only left for intervention is the penumbra/ischemic area,which treatment depend on the normalization  of the risk factor influencing (systemic) vascular con- dition

•         Up to the moment the what so called “neuro protective agents” has no evidence  proved  benefits (Penhall,2001)

•         Rehabilitation measures seem to be beneficial due to the brain plasticity

 

Viral Infections of Adenotonsil

Patients presenting with viral tonsillitis, usually simultaneously with viral pharyngitis, commonly complain of sore throat and difficulty swallowing. Upon examination, there is often fever and oropharyngeal erythema, usually without a tonsillar exudate. Viruses such as adenovirus, rhinovirus, reovirus, respiratory syncytial virus (RSV), and the influenza and parainfluenza viruses have all been shown to be possible pathogens. Most of these infections are self-limited and require only symptomatic treatment.

The Epstein-Barr virus (EBV) causes acute pharyngitis as a part of infectious mononucleosis syndrome. It is common in children and young adults, is transmitted by oral contact, and manifests as fever, generalized malaise, lymphadenopathy, hepatosplenomegaly, and pharyngitis. Upon examination, petechiae may be present at the junction of the soft and hard palates. The tonsils are severely enlarged, sometimes to the point of compromising the airway, and classically are covered with an extensive grayish-white exudate. A complete blood count (cbc) may be significant for lymphocytosis with atypical lymphocytes (activated T-cells). A Monospot test is more sensitive and specific than a heterophil antibody test, which can be negative in 10–15% of patients in the first week of illness. Treatment is largely supportive, with IV fluids and rest. In the case of progressive airway obstruction due to obstructive tonsillar swelling, a short course of systemic steroids can be very helpful. Rarely, a nasopharyngeal airway, nasotracheal intubation, or tracheotomy may be required to secure the airway.

Tonsillar infections with the Coxsackie virus result in herpangina, which presents as ulcerative vesicles over the tonsils, posterior pharynx, and palate. The disease commonly occurs in children under the age of 16. Patients present with generalized symptoms of headache, high fever, anorexia, and odynophagia.

Treatment for viral infections is mostly supportive, but the tonsils can have a bacterial superinfection that results in more severe symptoms. These patients can benefit from systemic antibiotics.

Acute Otitis Media

Essentials of Diagnosis

• Otalgia.
  
• Pyrexia.
  
• Thickened, bulging, hyperemic tympanic membrane.
  
• Hearing loss.
  
• ± Otorrhea.
  

Symptoms and Signs

Prior to the onset of symptoms of AOM, the patient frequently has symptoms of an upper respiratory tract infection. Older children will usually complain of earache, whereas infants become irritable and pull at the affected ear. A high fever is often present and may be associated with systemic symptoms of infection, such as anorexia, vomiting, and diarrhea. Otoscopy classically shows a thickened hyperemic tympanic membrane, which is immobile on pneumatic otoscopy.

Further progression of the infective process may lead to the spontaneous rupture of the tympanic membrane, resulting in otorrhea. If this occurs, the otalgia and fever often subside. At this stage, it is often not possible to visualize the tympanic membrane due to the discharge in the ear canal.

Otitis Media with Effusion

Otitis media with effusion may be completely asymptomatic and only detected on routine audiologic screening. The most common symptom of OME is hearing loss. While older children may complain of reduced hearing, in many cases the hearing loss is noticed by parents, a nursery nurse, or a teacher. In younger children, the only symptom may be delayed speech development or behavioral problems. Another common symptom is a "blocked" feeling in the ear, which may cause infants and young children to pull at their ears. More rarely, symptoms of earache, tinnitus, or balance disorder may be present.

Otoscopy classically reveals a dull gray- or yellow-colored tympanic membrane that has reduced mobility on pneumatic otoscopy. If the tympanic membrane is translucent, an air-fluid level or small air bubbles within the middle ear effusion may be seen

Pathogenesis of Sinusitis

The anatomy of the sinuses does not promote passive gravitational drainage and therefore the cilia of the sinonasal mucosa must function properly. Without the constant movement of mucus from the sinuses into the nose, accumulation and eventual infection is inevitable. This fact is illustrated by disorders such as Kartagener syndrome, in which ciliary movement is abnormal.

The cilia of the maxillary sinus propel mucous toward the natural ostia of the sinus, explaining why large openings made into the maxillary antrum at places other than the natural ostia (eg, in the inferior meatus) are ineffective at draining the sinus.

Acute sinusitis may begin with edema of the nasal mucosa and the resultant blockage of the sinus ostia, which then results in stasis and infection. The most common organisms responsible for acute sinusitis include Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis. Depending on the geographic location, approximately one third of S. pneumoniae isolates are resistant to penicillin and one third of H. influenzae produce -lactamase. Nearly all isolates of M. catarrhalis produce -lactamase.

Chronic sinusitis arises from longstanding inflammation of the sinonasal mucosa and is often caused by bacteria different from the bacteria that produce acute sinusitis. Laboratory studies in which maxillary mucopus was cultured during endoscopic surgery showed a high percentage of coagulase-negative Staphylococci, Staphylococcus aureus, and Streptococcus viridans.

Corynebacterium and anaerobes were also isolated. Although coagulase-negative Staphylococcus is often considered a contaminant, the organism may have a pathologic role in chronic sinusitis. Also of note, the coagulase-negative Staphylococcus isolated displayed significant antimicrobial resistance. In other studies of chronic sinusitis bacteriology, a similar range of organisms was cultured except that Pseudomonas was identified in a significant number of the isolates. One half of these Pseudomonas isolates were resistant to quinolones.

Fungus may also infect the paranasal sinuses, causing a wide range of disease. Certain species, specifically Mucor, cause invasive fungal sinusitis. Invasive fungal sinusitis is typically seen in the diabetic or immunocompromised patient and is characterized by a rapidly progressive course. The skull base and orbit are frequently involved, necessitating aggressive surgical and medical management. Fungus can also stimulate an immune response from the sinonasal mucosa, resulting in allergic fungal sinusitis. Typically, polypoid tissue is seen anterior to a mass consisting of mucin, fungal elements, Charcot-Leyden crystals, and eosinophils. Sinus expansion and bony remodeling are hallmark features of this process. Even though this is not an invasive, infectious process, the treatment is surgery with immunotherapy as a critical adjunct.

Acute ‘cold’ leg

Important diagnostic features

Isolated arterial embolus
• Sudden-onset, severe ischaemia, no previous symptoms of
vascular disease, previous history of atrial fibrillation/recent
myocardial infarction, all peripheral pulses on the unaffected
limb normal (suggesting no underlying peripheral vascular disease
[PVD]).
• Limb usually acutely threatened due to complete occlusion
with no collateral supply.
• Common sites of impaction are: popliteal bi(tri)furcation, distal
superficial femoral artery (adductor canal), origin of the profunda
femoris. ‘Saddle’ embolus at aortic bifurcation causes
bilateral acute ischaemic limbs.

Trauma
• May be due to direct injury to the vessel or by secondary compression
due to bone fragments or haematoma.
• Direct injuries may be due to: complete division of the vessel,
distraction injury, damage and in situ thrombosis, foreign body,
false aneurysm.

Thrombosis (in situ)
• Usually associated with underlying atheroma predisposing to
thrombosis after minor trauma or immobility (after a fall or illness).
• May be subacute in onset, previous history of known vascular
disease or intermittent claudication, associated risk factors for
peripheral vascular disease, abnormal pulses in the unaffected
limb.
• Paradoxically, the limb may not be as acutely threatened as in
isolated arterial embolus since collateral vessels may already be
present due to underlying disease.

Graft thrombosis
Often subacute in onset, limb not acutely threatened, progressive
symptoms, loss of graft pulsation

Aneurysm thrombosis
• Commonest sitebpopliteal aneurysms.
• Sudden-onset limb ischaemia, acutely threatened, may be
associated embolization as well, non-pulsatile mass in popliteal
fossa, many have contralateral asymptomatic popliteal aneurysm.

THE PARTOGRAPH

Partograph is a graphic that use for monitoring the 1st stage of the labor. The WHO partograph has been modified to make it simpler and easier to use. Thelatent phase has been removed, and plotting on the partograph begins in the active phase when the cervix is 4 cm dilated. Record the following on the partograph:

Patient information: Fill out name, gravida, para, hospital number, date and time of admission, and time of ruptured membranes OR time elapsed since rupture of membranes (if rupture occurred before charting on the partograph began).
Fetal heart rate: Record every half hour.
Amniotic fluid: Record the color of amniotic fluid at every vaginal examination: I: membranes intact; R:membranes ruptured; C: membranes ruptured, clear fluid; M: meconium-stained fluid; B: blood-stained fluid.
Molding: 1: sutures apposed; 2: sutures overlapped but reducible; 3: sutures overlapped and not reducible.
Cervical dilation: Assessed at every vaginal examination and marked with a cross (X). Begin plotting on the partograph at 4 cm.
Alert line: A line starts at 4 cm of cervical dilation to the point of expected full dilation at the rate of 1 cm per hour.
Action line: Parallel and 4 hours to the right of the alert line.
Descent assessed by abdominal palpation (Figure 4-1, below): Refers to the part of the head (divided into five parts) palpable above the symphysis pubis; recorded as a circle (O) at every abdominal examination. At 0/5, the sinciput (S) is at the level of the symphysis pubis.
Hours: Refers to the time elapsed since onset of active phase of labor (observed or extrapolated).
Time: Record actual time.
Contractions: Chart every 30 minutes; count the number of contractions in a 10-minute time period, and their duration in seconds.
Less than 20 seconds:
Between 20 and 40 seconds:
More than 40 seconds:
Oxytocin: Record the amount of oxytocin per volume IV fluids in drops per minute every 30 minutes when used.
Drugs given: Record any additional drugs given.
Pulse: Record every 30 minutes and mark with a dot (ﾁœ).
Blood pressure: Record every 4 hours and mark with arrows.
Temperature: Record every 2 hours.
Protein, acetone, and volume: Record when urine is passed.

Assist in Normal Birth

Clean the woman’s perineum with a cloth or compress, wet with antiseptic or soap and water, wiping from front to back.
Ask the woman to pant or give only small pushes with contractions as the baby’s head is born.

As the pressure of the head thins out the perineum, one way to control the birth of the head is with the fingers of one hand applying a firm, gentle downward (but not restrictive) pressure to maintain flexion, allow natural stretching of perineal tissue, and prevent tears.
Use the other hand to support the perineum using a compress or cloth, and allow the head to crown slowly and be born spontaneously. Do not manipulate the labia or perineum over the baby’s head because this increases the risk of tears.
Wipe the mucus (and membranes, if needed) from the baby’s mouth and nose with a clean cloth. Feel around the baby’s neck to ensure that the umbilical cord is not around it:
If the cord is around the neck but is loose, slip it over the baby’s head.
If the cord is loose but cannot reach over the head, slip it backwards over the shoulders.
If the cord is tight around the neck:
Tie or clamp the cord in two places 2 cm apart.
Cut the cord between the ties/clamps.
Unwind the cord from around the baby’s neck and proceed.