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Saturday, August 29, 2015

CAUSES, SYMPTOMS AND TREATMENT OF DENTAL ABCESS


What is dental abcess?
Dental abscess: An lesion characterized by localization of pus in the structures that
surround the teeth, can be either acute or chronic.
Sometimes the abscess develops some distance away from the teeth (like cervical region)
but if is of dental origin then still is called dental or odontogenic abscess.
When dental caries is not treated by restoration will results into pulpitis.
If pulpitis is not treated by root canal or extraction ends up with periapical abscess.
The periapical abscess and its counterpart periodontal abscess (due to periodontal
diseases) when extend out of the tooth boundaries may extend through the bone and
muscles causing pus collection in soft tissues which is called abscess.

Aetiology of Dental Abscess
Odontogenic (dental) infections are polymicrobial.
On average 4-6 different bacteria species are involved.
The normal flora bacteria are involved but the dominant isolates are anaerobes.
Generally the Anaerobic Gram negative rods followed by Anaerobic Gram positive cocci
are of significant concern.
The predominant species include; Bacteroides, Fusobacterium, Peptococcus,
Peptostreptococcus and Streptococcus viridians.
The abscess formation depends on loss of balance between the resistance of the host
tissues and virulence of bacteria.
When there is high resistance of host tissues with normal or low virulence of microbes
inflammation is usually confined, and resolve, otherwise abscess develops.
Common causes of entry of microbes and abscess formation include.
o Infected teeth e.g. deep caries, trauma involving the pulp.
o Periodontal infections.
o Pericoronitis is a common condition, and is an infection of the gingiva surrounding a
partially erupted third molar.
o Post-extraction infection – (especially in septic procedures).
o Introducing infection by a needle during administration of local anaesthesia especially
mandibular block.
o Mandibular and maxillary fractures.

Clinical Features of Dental Abscess
Patient looks moderately ill sometimes severely ill and toxic.
High body temperature.
Painful swelling.
The skin is tense, shiny, warm and red or purple unless the abscess is very deep.
Muscle trismus (the patient is unable to open his/her mouth fully).
Gingival fistulas (drainage of pus into the mouth).
Cellulitis (inflammation of the soft tissues).

Extension of Dental Abscess
The dental abscess usually extend to the following regions/spaces; buccal space,
sublingual, submental, submandibular and generally around the mandible and maxilla.
Sometimes the infection can extend to distant areas like cervical, pharynx and
mediastenum on the inferior aspect, infraorbital, parotid and temporal superioly.
Life threatening infections due to complications of dental abscess include:
o Ludwing’s angina(bilateral swelling of the submandibular and submental spaces
includind floor of the mouth causing rising of the tongue and airway obstruction).
o Mediastinitis; infection descending from orofacial region to cervical and eventually to
the chest.
o Carvenous sinus thrombosis:- infection ascends to the carvenous sinus and can cause
thrombosis with the sinus and and meningitis.

Treatment of Dental Abscess
Antibiotics
Combination of broad spectrum antibiotics of penicillin family or its alternative with
metronidazole (highly active against anaerobic gram-negative bacilli).

Analgesics and Antipyretics
Non-streroidal ant-inflammatory drugs (NSAIDs) like ibuprofen and diclofenac are
useful to relieve pain and reduce fever.

Incision and Drainage and Removal of the Cause
This is the ideal treatment of abscess once pus has been localized.
The dental personnel around can be of help to the patient, if there is none patient shoud be
referred immediately after providing basic care like antibiotics and analgesics.
Removal of the cause may mean extraction of an offendind tooth which is done during
incision and drainage where feasible if not then few day later. Note: Always Make Sure You Assess the Airway

Some forms of dental abscess cause life threatening airway obstruction ( e.g. Ludwig’s
agina).In such case endotracheal intubation or trachestomy may be required.

Ludwig’s Angina
A bacterial infection of the floor of the mouth
Swelling of the tissues occurs rapdily and may block the airway or prevent swallowing of
saliva.
Symptoms include
o Breathing difficulty
o Confusion or other mental changes
o Fever
o Neck pain
o Neck swelling
o Redness of the neck
o Weakness, fatigue, excessive tiredness
o Drooling
o Earache
Signs include
o An examination of the neck and head shows redness and swelling of the upper neck,
and under the chin.
o The swelling may reach to the floor of the mouth.
o The tongue may be swollen or out of place

Complications of Dental Abscess
Osteomyelitis of the jaws
Maxillary sinusitis
Cavernous sinus thrombosis
Necrotizing fasciitis
Others:
o Mediastinitis
o Meningitis
o Brain abscess

General Pre-referral Care for Dental Patients
Patient with pain due to pulpitis or any other cause are given analgesics
Patient with acute infections are given antibiotics and analgesics
Patient with acute infections are assessed for danger of airway obstruction and toxaemia
Patients with traumatic dental injuries are given analgesics and antibiotics
Patients with bleeding effort is made first to control bleeding by packing with a gauze
(preferably soaked with adrenaline) and if persist suturing is attempted.If bleeding persists then pack the site, stabilize the patient with intravenous fluids (and
blood if patient has bled a lot) and refer
Always insist on abiding to the referral plan

Wednesday, August 26, 2015

CAUSES, TREATMENT AND PROGNOSIS OF NEPHROTIC SYNDROME.


what is nephrotic syndrome?
Nephrotic syndrome: A clinical complex characterized by a number of renal and extrarenal
features.
The most prominent features are
o Proteinuria of >3.5g per 24 hours (in practice, >3.0 to 3.5 g per 24 h)
o hypoalbuminemia
o Edema
o Hyperlipidemia
o Lipiduria
o Hypercoagulability

It should be stressed that the key component is proteinuria which results from altered
permeability of the glomerular filtration barrier for protein.
The other components of the Nephrotic syndrome and the ensuing metabolic
complications are all secondary to urine protein loss and can occur with lesser degrees of
proteinuria or may be absent even in patients with massive proteinuria.

Causes of Nephrotic Syndrome
There are many specific causes of nephrotic syndrome.
In all cases injury to glomeruli is an essential feature.
Nephrotic syndrome may affect adults and children of both sexes and of any race.
It may occur in typical form or in association with nephritic syndrome.
The latter connotes glomerular inflammation with hematuria and impaired kidney
function.
 Primary Causes of nephrotic syndrome
o Minimal-change nephropathy
o Focal glomerulosclerosis
o Membranous nephropathy
o Hereditary nephropathies either primary and or secondary causes.

Secondary Causes
Being a renal manifestation of a systemic general illness
o Diabetes mellitus (DM)
o Systemic lupus erythematosus (SLE)
o Amyloidosis and paraproteinemias
o Viral infections (e.g. hepatitis B, hepatitis C, HIV)
o Pre-eclampsia

Other Causes
Medication can cause nephrotic syndrome.
This includes the very infrequent occurrence of minimal-change nephropathy with
NSAID use i.e aspirin and the occurrence of membranous nephropathy with the administration of
gold and penicillamine which are older drugs used for rheumatic diseases.

Pathophysiology
Proteinuria that is more than 85% albumin is selective proteinuria.
Albumin has a net negative charge and it is proposed that loss of glomerular membrane
negative charges could be important in causing albuminuria.
Nonselective proteinuria being a glomerular leakage of all plasma proteins would not
involve changes in glomerular net charge but rather a generalized defect in permeability.
This construct does not permit clear-cut separation of causes of proteinuria except in
minimal-change nephropathy in which proteinuria is selective.

Pathogenesis of Oedema
An increase in glomerular permeability leads to albuminuria and eventually to
hypoalbuminemia.
In turn hypoalbuminemia lowers the plasma colloid osmotic pressure causing greater
transcapillary filtration of water throughout the body and thus the development of edema

Metabolic Consequences of Proteinuria
In nephrotic syndrome levels of serum lipids are usually elevated.
The loss of antithrombin III and plasminogen via urine along with the simultaneous
increase in clotting factors especially factors I, VII, VIII and X increases the risk for
venous thrombosis and pulmonary embolism.
Vitamin D binding protein may be lost in the urine leading to hypovitaminosis D with
malabsorption of calcium and development of bone disease.
Urinary immunoglobulin losses may lower the patient's resistance to infections and
increase the risk of infections.

Clinical Features of Nephrotic Syndrome
History
The first sign of nephrotic syndrome in children is usually swelling of the face followed
by swelling of the entire body.
Adults can present with dependent edema.
Foamy urine may be a presenting feature.
A thrombotic complication such as deep vein thrombosis of the calf veins or even a
pulmonary embolus may be the first clue indicating Nephrotic syndrome.
Additional historical features that appear can be related to the cause of Nephrotic
syndrome.
Recent start of a non steroidal anti-inflammatory drug (NSAID) or a 10-year history of
diabetes may be very relevant.

Physical
Edema is the predominant feature of nephrotic syndrome and initially develops around
the eyes and legs.
With time edema becomes generalized and may be associated with an increase in weight
and development of ascites or pleural effusions.
Haematuria and hypertension manifest in a minority of patients.
Additional features on exam will vary according to the cause and as a result of whether or
not renal function impairment exists.
In cases of longstanding diabetes there may be diabetic retinopathy which correlates
closely with diabetic nephropathy.
If the kidney function is reduced there may be hypertension and/or anemia

Differential Diagnoses
Diabetic nephropathy
Focal segmental glomerulosclerosis
Glomerulonephritis
HIV nephropathy
IgA nephropathy
Minimal change kidney disease
Light chain-associated renal disorders
Nephritis
Radiation
Sickle cell nephropathy
Heart failure
Liver cirrhosis with portal hypertension

Investigations
Perform dipstick screening method for detection of protein concentrations in urine.
The dipstick is a quick method of screening and detecting proteinuria, hematuria, and
pyuria and provides an estimate of the specific gravity (urine-concentrating capacity).
More laboratory investigations can be done at higher centers.

Laboratory Studies
Urinalysis is the first test used in the diagnosis of Nephrotic syndrome
Nephrotic range proteinuria will be apparent by 3+ or 4+ readings on the dipstick or by
semi quantitative testing by sulfosalicylic acid
A 3+ reading is 300 mg/dl of urinary protein or more which is 3 g/l or more and thus in
the Nephrotic range
The chemistry of the dipsticks is such that albumin is the major protein that is tested
The urine sediment exam may show cells and/or casts
The presence of more than 2 red blood cells (RBCs) per high power field is indicative of
microhematuria
Urinary protein is measured by a timed collection or a single spot collection
In healthy individuals there are no more than 150 mg of total protein in a 24-hour urine
collection
A single spot urine collection is much easier to obtain
Serum tests for kidney function are essential
Serum creatinine will be in the normal range in uncomplicated nephrotic syndrome such
as that occurring in minimal-change nephropathy
The serum albumin is classically low in nephrotic syndrome being below its normal range
of 3.5-4.5 g/dl

Imaging Studies
Ultrasonographic
Scanning can be used to determine whether a patient possesses 2 kidneys and to
demonstrate their echogenicity.
Note: Individuals with a single kidney may be prone to developing focal glomerulosclerosis.
Having only one kidney is also a relative contraindication to kidney biopsy.

Treatment
Acute Management of Adult Nephrotic Syndrome
o The principles for acute management of adults with nephrotic syndrome are similar to
those for children.
o Diuretics will be needed such as Furosemide, Spironolactone and even Metolazone
may be used.
o Volume depletion may occur with diuretic use which should be monitored by
assessment of symptoms, weight, pulse and blood pressure.
o Anticoagulation has been advocated by some for use in preventing thromboembolic
complications but its use in primary prevention is of unproven value.
o Hypolipidemic agents may be used but if the nephrotic syndrome cannot be controlled
there will be persistent hyperlipidemia.
o In secondary Nephrotic syndrome such as that associated with diabetic nephropathy,
angiotensin-converting enzyme (ACE) inhibitors and/or angiotensin II receptor
blockers are widely used.

Specific Treatment of Nephrotic Syndrome
Depends on the disease's cause.
Glucocorticosteroids such as prednisone are used for minimal-change nephropathy.
Prednisone and cyclophosphamide are useful in some forms of lupus nephritis.
Secondary amyloidosis with Nephrotic syndrome may respond to anti-inflammatory
treatment of the primary disease.

Diet
For patients with Nephrotic syndrome their diet should provide adequate energy (caloric)
intake and adequate protein (1-2 g/kg/d).
Supplemental dietary protein is of no proven value.
A diet with no added salt will help to limit fluid overload.
Management of hyperlipidemia could be of some importance if the Nephrotic state is
prolonged.
Fluid restriction per se is not required.

Activity
There are no activity restrictions for patients with Nephrotic syndrome
Ongoing activity rather than bed rest will reduce the risk of blood clots
Complications
Infection is a major concern in nephrotic syndrome.
Atherosclerotic vascular disease appears to occur in greater frequency in subjects with
nephrotic syndrome than in healthy subjects of the same age.
Hypocalcemia is common in nephrotic syndrome but rather than being a true
hypocalcemia it is usually caused by a low serum albumin level.
Venous thrombosis and pulmonary embolism are well known complications of nephrotic
syndrome.
Hypovolemia is generally observed only when the patient's serum albumin level is less
than 1.5 g/dl.
Acute renal failure may indicate an underlying glomerulonephritis but is more often
precipitated by hypovolemia or sepsis.
Hypertension related to fluid retention and reduced kidney function may occur.
Failure to thrive (in children) may develop in patients with chronic edema including
ascites and pleural effusion.

Prognosis
The prognosis for patients with primary nephrotic syndrome depends on its cause.
The prognosis with congenital nephrotic syndrome is poor and survival beyond several
months is possible only with dialysis and kidney transplantation.
Only about 20% of patients with focal segmental glomerulosclerosis undergo remission
of proteinuria. An additional 10% improve but remain proteinuric.
Many patients experiencing frequent relapses become steroid-dependent or become
steroid-resistant.
End-stage renal disease develops in 25-30% of patients with focal segmental
glomerulosclerosis (FSGS) by 5 years and in 30-40% of these patients by 10 years.
The prognosis for children with minimal-change nephropathy is very good.


 
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