Dec 31, 2018

Diabetic Ketoacidosis (DKA) definition, symptoms, diagnosis, treatement

Definition: DKA is a potentially fatal acute metabolic complication of diabetes mellitus. It is characterized by the biochemical triad of hyperglycemia, ketonemia, and metabolic acidosis.

DKA is typically associated with type 1 diabetes but may also occur in type 2 diabetes during periods of infection, trauma, cardiovascular injury, or other emergencies. It is more common in young people with type 1 diabetes and in females. It may be the presenting manifestation of diabetes.

Precipitating factors

  • Inadequate dosing of insulin
  • Cardiovascular disorders (myocardial infarction, stroke)
  • Infection.
  • Drug use (steroids, diuretics, vasopressors, antipsychotics, cocaine).


DKA results from severe alterations in carbohydrate, protein, and lipid metabolism. In simple terms, it is the consequence of severe cell starvation and death resulting from a relative or complete deficiency of insulin needed to transport glucose into the cells. Increased gluconeogenesis, increased glycogenolysis, and decreased use of glucose by the muscles, liver, and fat lead to profound metabolic derangements. Insulin deficiency promotes lipolysis. Lipolysis also plays a key role in promoting metabolic decompensation by providing the substrate for the formation of ketone bodies (acetone, beta-hydroxybutyric acid, and acetoacetic acid). Decreased clearance of ketone bodies leads to ketonemia and results in an anion gap metabolic acidosis. There are also elevated levels of proinflammatory cytokines and procoagulant factors (C-reactive protein and interleukin-6 and -8) that predispose the patient to thrombosis.

Clinical Manifestation and Diagnosis

Severe disease can develop in less than 24 hours after the onset of ketosis.Clinical manifestations include:
  • Polyuria, polydipsia, polyphagia, and weakness.
  • Manifestation of dehydration (dry mucous membranes, flattened neck veins, tachycardia, hypotension, and orthostasis).
  • Nausea and vomiting are common, occurring in up to 80% of patients.
  • A fruity odor to their breath, resulting from elevated serum acetone.
  • Kussmaul respirations (rhythmic, gasping deep respirations with normal or reduced frequency). as a compensatory response to the underlying metabolic acidosis seen in this disorder.
  • Altered mental status. The spectrum can vary from mild confusion to coma.

N.B. In short, DKA is nearly universally associated with  profound intravascular volume depletion and restoration of this is a cornerstone of therapy.


  1. Serum ketones
  2. Widened anion gap metabolic acidosis.
  3. Hyperglycemia is almost always seen but is not required for the diagnosis, and clinically significant DKA can occur in patients with normal serum glucose levels.
  4. Most patients have elevations in the blood urea nitrogen and serum creatinine concentration,
  5. Hyponatremia results from the osmotic diuresis
  6. Hyperkalemia results from insulin deficiency
  7. Hemoglobin A1C measurement may be useful in determining whether the episode is an acute exacerbation of previously controlled diabetes or the first manifestation of undiagnosed diabetes. However, level of hemoglobin A1C should not be relied on to diagnose or initiate treatment for DKA.
  8. Evaluation for underlying infectious causes should be undertaken because of the common associations with DKA.

Treatment strategies

  • Normalization of the serum glucose and electrolytes(especially in potassium, magnesium, and phosphorous).
  • Restoration of the intravascular volume.
  • Resolution of the metabolic acidosis (closure of the anion gap).
  • Treatment of the precipitating factor e.g.sepsis.



  • An initial intravenous bolus of regular insulin at 0.1 U/kg body weight
  • Followed by a continuous infusion of regular insulin at a dose of 0.1 U/kg/hour.
  • Long-acting and oral preparations should be strictly avoided during the initial treatment of this disorder as rapid fluctuations in serum glucose levels may be experienced and are more easily managed with regular insulin.
  • The insulin drip should be continued until the anion gap closes and not when the serum glucose level normalizes.
  • Glucose should initially be measured hourly, with appropriate adjustments to the insulin drip. If the serum glucose level becomes normal or low in the face of a persistently widening anion gap
  • Intravenous dextrose should be given and the insulin drip rate reduced but not stopped.

Initial fluid therapy

  • Up to 6 liters to adequately replete intracellular volume.
  • Caution must be taken during fluid repletion as rapid reduction in plasma osmolality can precipitate cerebral edema.
  • Isotonic saline is the initial resuscitative fluid of choice.

- Rate= 15-20 mL/kg/hour for the first several    hours.
- Once the serum glucose level is below 200-250 mg/dL, the fluids should be changed to one-half normal saline with dextrose (D5 1/2NS). 

N.B.   Fluid therapy &insulin infusion should be continued till normalization of anion gap (reflects recovery from metabolic acidosis).

Causes of death in Diabetic Ketoacidosis

  • Cerebral edema.
  • Shock.
  • Electrolyte abnormalities (esp hypokalemia induced by insulin therapy).
  • The underlying precipitant for DKA, especially sepsis. 


DKA is preventable complication of diabetes ,so patients must be educated about insulin compliance and encouraged to seek medical attention in the early coarse of illness. 

Correction of hypokalemia induced by insulin infusion in treatment of DKA

    Normal serum k+ -----------(3.5 - 5 meq/L)
  • Serum k+ is measured every hour during treatment of DKA
  • amount of k+ given is determined according to serum k+ level
serum k+ (meq/l)                  amount of k+ given (meq)

     < 3                                                 40
     3 - 4                                               30
     4 - 5                                               20
     5 - 6                                               10
     > 6                                                 0
Monitoring of serum k+ is continued every hour even after stoppage of  k+ administration to avoid recurrent hypokalemia

N.B. Due to hyperosmolarity of k+ solution ,it must be diluted.

Adrenal Insufficiency, Addison's disease, Addison's Crisis

Definition: Acute adrenal crisis is an extreme life-threatening manifestation of adrenal insufficiency. It occurs secondary to interruption of a normal or hyperfunctioning adrenal or pituitary gland or sudden interruption of adrenal replacement therapy.

Adrenal insufficiency can be divided into 3 categories:
  1.  chronic primary adrenal insufficiency (Addison disease)
  2.  chronic secondary adrenal insufficiency
  3.  and adrenal crisis (acute adrenal insufficiency).

Addison disease 

       causes :
  • Autoimmune in 80 % of cases
  • Infections (T.B. , HIV)
  • Metastases

 Chronic secondary adrenal insufficiency (-- ACTH)

caused by pituitary tumour

Adrenal crisis

 causes :
  • Sudden withdrawal of chronic steroids usage (or secondary to stress)
  • Adrenal hge (caused by,meningiococci-sepsis-warfarin therapy-coagulopathy)
  • Pituitary dysfunction (sheehan syndrome)
  • CNS lesions in rare cases         

Clinical manifestations of adrenal crisis

  • Unexplained hypotension (resistant to fluid and catecholamines)  
  • nonspecific symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion, or coma.


Immediate treatment of adrenal crisis should begin prior to laboratory confirmation (usually hyperkalemia,hyponatremia)

  • Normal saline is the intravenous fluid of choice
  • Stress-dose steroid replacement should be administered. Hydrocortisone may be administered as a 100-mg intravenous push followed by continuous infusion of 150-300 mg/day for 2 to 3 days
  • Alternatively, dexamethasone as a 4-mg intravenous bolus may be administered instead of hydrocortisone to avoid interference with testing of cortisol levels
  • Mineralocorticoid, namely fludrocortisone acetate, should also be administered at 0.1 mg daily. 

Dec 30, 2018

Deafness definition, types and causes of hearing loss

Definition: It means diminution of hearing up to complete loss, in other words: it is total or partial inability to hear sounds.
Types: There are Organic and Hysterical causes of deafness, Organic typre is classified into 3 sub-categories as discussed below.
I. Organic: A: Conductive. B: perceptive (SNHL). C: mixed.
II. Hysterical.

A. Conductive hearing loss

It means interference of sound transmission along the conductive apparatus (External & middle ear).

I. Causes in the External Auditory Canal (EAC):

II. Causes in the Tympanic membrane:

III. Causes in the Middle Ear:

IV. Causes in Eustachian tube:

  • Congenital: cleft palate.
  • Traumatic: post adenoidectomy scarring, barotrauma.
  • Inflammatory: tubal catarrh.
  • Neoplastic: nasopharyngeal tumors.
  • Miscellaneous: hypertrophy of the adenoid.

B - Sensorineural hearing loss

It means defect in conversion of sound energy to electrical impulses (cochlea) or transfer of impulses along cochlear nerve & central connections to auditory cortex.

I. Cochlear Causes (Sensory):

a. Congenital: Hearing loss dating since birth or shortly after.

1. Hereditary due to genetic aberrations:
  • If Deafness alone:

Michael’s: total lack of inner ear development.
Mondini’s: partial aplasia of labyrinth cochlea makes 1 ½ turns.
  • If Deafness with other abnormalities:
Usher’s Syndrome: SNHL + retinitis pigmentosa.
Pendred’s Syndrom: SNHL + goitre.
Alport’s Syndrome: SNHL + nephritis.

2. Prenatal:
  • Maternal infections as rubella in the 1st trimester.
  • Drug intake in the 1st trimester e.g. quinine, aminoglycosides and salicylates.
3. Natal: (during labour): 
  • Hypoxia or anoxia of the fetus.
  • Birth trauma as in forceps delivery.
4. Postnatal:
  • Neonatal infections.
  • Erythroblastosis foetalis (Rh incompatibility).

b. Traumatic

  • Transverse fracture of temporal bone involving the labyrinth.
  • Labyrinthine membrane rupture(perilymph fistula).
  • Acoustic (noise) trauma.

c. Inflammatory (Labyrinthitis)

1- Infective:
  • Viral: measles, mumps, influenza, the deafness occurs after the febrile stage. It may be unilateral or bilateral, asymmetric and affects more the high tones.
  • Syphilitic labyrinthitis: deafness is progressive, asymmetric and may be associated with vestibular symptoms (i.e. Vertigo).
  • Bacterial: - Labyrinthitis secondary to suppurative otitis media, Meningitis: deafness is bilateral and profound.
2- Toxic:
  • Ototoxic drugs: quinine, aminoglycosides, salicylates, and Lasix.
  • Metabolic: uremia, diabetes, thyrotoxicosis.

d. Vascular

Internal auditory artery occlusion due to spasm, thrombosis or embolism.
It causes sudden hearing loss (treated by large dose of steroids).

e. Miscellaneous

  • Presbycusis (senile deafness).
  • Meniere’s disease.
  • Pure cochlear otosclerosis.
  • Perilymph fistula.

II. Retrocochlear causes

Due to lesion either in the vestibulocochlear nerve, or in the auditory pathway.

1- Vestibulocochlear nerve affection:
A- Cerebellopontine angle lesions as in acoustic neuroma, and congenital cholesteatoma.
B -Meningitis.
C-Vascular loop.

2 - Central: due to lesion anywhere in the auditory pathway. It is rare.
A-Multiple sclerosis.
B-Meningitis, encephalitis.
C- Brain tumours.
D-Cerebrovascular accidents e.g. thrombosis, haemorrhage or embolism.

C - Mixed Hearing Loss

1- Congenital meatal atresia with inner ear anomaly.
2- Fracture base of skull.
3- Complicated CSOM with labryinthitis.
4- Combined otosclerosis i.e. (footplate fixation, cochlear otosclerosis).

Acoustic Neuroma: definition, incidence, symptoms, investigations and treatment

Definition: Benign tumor arises from schwann cells of vestibular n. (vestibular schwannoma).
Incidence: 40-50 years age of presentation. 8% of brain tumors,80% of CPA.


 Arise from glial neurilemmal junction at IAM (or CPA).
Grossly: slowly growing, encapsulated, smooth, and firm.
MP: Fasiculated type (Antoni A), Reticular (Antoni B).

Clinical picture of Acoustic Neuroma

A) Otological:
  • Unilateral slowly progressive SNHL.
  • Unilateral tinnitus.
  • Vertigo is not marked as condition is slowly progressive, allows for central compensation.
B) Neurological:
  • Lost corneal reflex. 
C) Cerebellar
D) Terminal:
  • Increased intra-cranial tension and death.

Investigations for diagnosis of Acoustic Neuroma

  • PTA : reveals SNHL.
  • Speech audiogram: poorer speech discrimination than PTA (retrocochlear lesion).
  • ABR delay of wave V.
  • CT with contrast.
  • MRI with contrast: the best.

Differential diagnosis of Acoustic Neuroma

Other CPA lesions, e.g Meningioma, congenital cholesteatoma, arachnoid cyst, and pontine glioma.

Treatment of Acoustic Neuroma

  •  Surgery: approach depends on size and hearing.
  • Small intracanalicular tumor with good hearing….middle cranial fossa.
  • Large CPA tumors with good hearing……….retrosigmoid.
  • Bad hearing ….translabrynthine.
  • Gamma knife (stereotactic radio surgery).

Dec 16, 2018

Meniere’s disease| causes, symptoms, signs, diagnosis and treatment

Meniere’s disease is a disorder of vestibular labyrinth characterized by triad of paroxysmal vertigo, deafness & tinnitus due to increased volume & pressure of endolymph.
In brief: - Endolymphatic hydrops with attacks of low frequency SNHL, tinnitus, vertigo and sensation of ear fullness.

- In between attacks the patient is usually symptom free. However, the patient may present later with progressive SNHL that is detectable by audiogram even in absence of the attack.
- There’s no specific test to confirm the diagnosis. It’s usually based on the clinical findings, audiogram findings and electrocochleogram to confirm the hydrops.
- Medical treatment is the usual role. Surgery is very rarely needed and is mainly about endolymphatic sac decompression +/- shunting.

Causes of Meniere’s disease

The cause of Meniere's disease isn't understood. One popular theory that hasn't been proved is that Meniere's disease appears to be the result of the abnormal amount of fluid (endolymph) in the inner ear. Disorders that may give rise to elevated endolymphatic pressure include:
  • Metabolic disturbances.
  • Hormonal imbalance.
  • Trauma.
  • Various infections eg, otosyphilis and Cogan’s syndrome [interstitial keratitis].
  • Autoimmune diseases, such as lupus and rheumatoid arthritis, may cause an inflammatory response within the labyrinth. An autoimmune etiology was postulated after there was found to be an association with the presence of thyroid autoantibodies in patients with Meniere’s disease.
  • In addition, allergy has been implicated in many patients with difficult-to-treat Meniere’s disease. Food triggers are also important factors in the generation of hydrops.


  • Meniere’s disease appears to be more common in females than in males.
  • Meniere’s disease can be seen at almost all ages, but it usually starts between the ages of 20 and 50.
  • The female predilection of Meniere’s disease is shared with migraine headache and, in fact, there is a growing body of evidence that Meniere’s disease and migraine headache may be related and/or different spectrums of the same disease.

Clinical presentation (manifestations):

Ménière disease is defined as “recurrent, spontaneous episodic vertigo; hearing loss; aural fullness; and tinnitus. Either tinnitus or aural fullness (or both) must be present on the affected side to make the diagnosis.


  • Vertigo is a subjective sensation of motion while motionless.
  • Horizontal or rotatory nystagmus is always present during vertiginous attacks.
  • The vertiginous attacks may last from minutes to hours and often are associated with severe nausea and vomiting.
  • At least 2 definitive episodes of vertigo of at least 20 minutes duration must have occurred to make the diagnosis.
  • In 10% of patients with the symptom of vertigo, Ménière disease is the cause.
  • Between episodes, some patients are completely symptom free. Many notice progressive deterioration of hearing and balance function with each successive attack.

Hearing loss

-Sensorineural hearing loss must be documented audiometrically in the affected ear at least once during the course of the disease. There may be fluctuation in the degree of hearing loss superimposed on a gradual decrement in function.
-The hearing loss primarily affects low frequencies.


Tinnitus is often nonpulsatile and may be described as whistling, although the classic description is that of low-tone, ocean-like roaring.
- It may be continuous or intermittent, usually corresponding to the loss of hearing during the attack.


In 50%: ear fullness, otalgia & increase tinnitus.

Signs of Meniere’s disease:

- Normal tympanic membrane.
- Tuning fork: P.D.

Investigations to diagnose Meniere’s disease

1- PTA: SNHL (see above).
2- Speech audiogram: poor discrimination matching PTA.
3- Electro cochleography: diagnostic.
4- Dehydration (Glycerol) test: during the attack PTA >> 1.5 mg/kg glycerin + equal saline >> PTA after 3h.: if improved by 10-15 dB (+ve).
5- Caloric test: hypoactive labyrinth (canal paresis).
6- CT to exclude retrocochlear pathology. 


Treatment of Meniere’s disease

A. Medical ttt:

Medical therapy can be directed toward treatment of the actual symptoms of the acute attack or directed toward prophylactic prevention of the attacks. 
Most care in the emergency department (ED) is based on symptomatic relief of the clinical findings.

-Salt-restricted diet, steroids, and the use of diuretics are often first-line therapies
-Intravenous (IV) or intramuscular (IM) diazepam provides excellent vestibular suppression and antinausea effects.
-Steroids can be given for anti-inflammatory effects in the inner ear.
-IV fluid support can help prevent dehydration and replaces electrolytes.
-Typically, vestibulosuppressants and antinausea medications (eg, meclizine,
-During the quiescent phase, medical treatment of Ménière disease is tailored to each patient. 

Lifestyle and dietary changes are usually the first step. Avoiding trigger substances (eg, salt, chocolate, caffeine) alone may be sufficient. Smoking cessation also is recommended. If medications are required, a 3-month trial of a diuretic (eg, hydrochlorothiazide/triamterene) and dietary management are prescribed.

Non invasive therapies

-Rehabilitation: If the patient has balance problems between episodes of vertigo, vestibular rehabilitation therapy might improve the balance.

-Hearing aid: A hearing aid in the ear affected by Meniere's disease might improve the hearing. Doctor can refer patient to an audiologist to discuss what hearing aid options that would be best for him.

-Meniett device: For vertigo that's hard to treat, this therapy involves applying pressure to the middle ear to improve fluid exchange. A device called a Meniett pulse generator applies pulses of pressure to the ear canal through a ventilation tube.

B. Surgical ttt

-Failed prolonged medical ttt.
- Progressive hearing loss.

A) Good (serviceable) hearing.
-Intratympanic injection of selective vestibulotoxic drugs.
-Endolymphatic sac decompression (Saccus decompression).
-Selective section of vestibular nerve.

B) Bad (non serviceable) hearing.
- Surgical labyrinthectomy (not done).
- Chemical labyrinthectomy (gentamycin).

Jul 25, 2018

Bell’s palsy| definition, causes, symptoms, signs and treatment

Bell’s palsy is the most common cause of facial nerve paralysis.
Deinition: (Lower motor neuron lesion) LMNL facial palsy.

What are the causes of Bell's palsy? 

Idiopathic (several theories).
1- Vascular ischaemia: local vasospasm of vasa nervosa >> oedema of nerve sheath >> nerve compression >> secondary ischaemia & more damage. 1ry ischaemia may be due to exposure to cold draughts.
2- Viral theory: isolated viral neuritis, single manifestation of polyneuritis,or reactivation of herpes simplex.

3- Auto immune.

Incidence: The commonest cause of LMNL, 80 – 90 %.

What are the symptoms and signs of Bell's palsy?

Clinical picture of Bell's palsy

It affects mainly middle aged adults, and affects both sexes equally. It may be precipitated by exposure, to cold air draughts, emotional stress, or pregnancy. The diagnosis of Bell’s palsy is made by exclusion of all other etiologies of facial paralysis.
It presents as:

1- Unilateral LMN facial paralysis of sudden onset, which may be partial or complete, and reaches a maximum in few days.
2- Retroauricular pain may occur several hours before the onset of the paralysis.
3- A reddish chorda tympani nerve may be visible through the posterosuperior part of the T.M.
4- Metallic taste and hyperacusis.


 usually it is a clinical diagnosis
  • In prolonged,or recurrent cases CT & MRI to exclude facial neuroma.
  • To detect the level.
  • Electrodiagnostic tests.

What is the treatment of Bell's palsy?

 most cases recover spontaneously.
1- General measures.
2- Medical treatment as early as possible:
  • a) Vasodilators in 1st few hours to relieve 1ry ischaemia e.g. nicotinic acid, histamine, beta histine.
  • b) Steroids (Medical nerve decompression):

To decrease edema & inflammation.
-Should be given early in tapering dose.
-Start with prednisolone 80mg / day.
-If no response after 2w give 2nd course.
  • C) Acyclovir (Zovirax): 200 mg 5 times daily for 10 days

3- Surgical decompression
Indication: > 90% degeneration after 2weeks.
Decompression by exposing bony canal & splitting the sheath from stylo mastoid foramen to level of compression.
4- Late cases: facial rehabilitation.

Jul 11, 2018

Facial nerve paralysis| symptoms, signs, leveling, complications, management

Facial palsy is a serious disorder with serious complications.
Causes of Facial nerve paralysis are discussed in details and figures here.

Pathology of facial paralysis

1- Neurapraxia:

- Definition: Functional conduction nerve block.
- Prognosis: Spontaneous complete recovery occurs within 1 - 4 weeks.

2- Wallerian degeneration:

a) Axonotmesis:

- Definition: Degeneration of the nerve axon, but the nerve sheath remains intact.
- Prognosis: The nerve axon grows inside the nerve sheath at a rate of 1 mm/day. Spontaneous recovery occurs, but is delayed (2-3 months) and maybe incomplete.

b) Neurotmesis:

- Definition: Degeneration of the nerve axon and nerve sheath.
- Prognosis: worst. Spontaneous recovery is always incomplete and delayed up to one year.

Clinical picture of facial paralysis

Depends on site of lesion.

A. Paralysis of muscles of the face (Motor):

  1. Inability to raise eye brow (occipito frontalis).
  2. Inability to close eyes firmly (orbicularis oculi).
  3. Inability to whistle (orbicularis oris).
  4. Food collects beneath cheek (buccinator).
  5. Deviation of angle of mouth to healthy side upon smiling, drooping of angle of month on affected side, dripping of saliva & loss of nasolabial fold (levator anguli oris).

B. Sensory and parasympathetic affection

  1. Affection of GSP: decreased lacrimation.
  2. Affection of nerve to stapedius: hyperacusis (disturbed hearing).
  3. Affection of chorda tympani: metallic taste.
  • Tone: by comparing both sides at rest.
  • Power: by comparing both sides during movement.
  • Degree: partial or complete paralysis.

Differentiation between UMN and LMN paralysis:

N.B: In UMN facial paralysis only the lower half of the face is paralyzed, this is because the upper part of the motor facial nucleus supplying the upper part of the face is bilaterally represented in the cerebral cortex.

Leveling of LMN facial paralysis:

According to presentation.

Investigations to confirm diagnosis:

A- To identify the cause:

  1. CT scans of brain and petrous bone to show fractures, cholesteatoma, or tumors.
  2. MRI petrous bone to show tumors especially facial neuroma.
  3. Audiogram (PTA).

B- To detect the level of the lesion:

  1.  Schirmer’s test (test for lacrimation): It is significant when the differences between the
    lacrimal flow of both sides exceed 30% of the total bilateral lacrimation, indicating a lesion at or above the geniculate ganglion.
  2. Stapedial reflex.
  3. Taste sensation:
a- Qualitative: compare taste of different staff applied to the lateral edge of the anterior 2/3 of the tongue.
b- Quantitative: electrogustometry.

4. Submandibular salivary flow test.

C- Electrophysiological studies:

Developed to evaluate the degree of facial nerve dysfunction, and the potential for recovery, they are used only in patients with complete paralysis.
They are: minimum nerve excitability test (NET), maximal stimulation test (MST), electroneuronography (ENoG), and electromyography (EMG).
Currently the 2 most helpful are: ENoG and EMG.
  1. Nerve excitability test: Determine the minimal electrical current in milliamperes required to produce a just visible muscle contraction, and compare both side, done 3 days after injury.
  2. Electroneuronography (ENoG), evoked electromyography:
  • This is the most important test.
  • Measurement of the amplitude of the summation action potentials of the muscles when a supramaximal stimulus is applied to the nerve and compare both sides.
  • This is important to detect the percentage of degeneration, which is important to decide the way of management and prognosis.
  • It is done after 2-3 days.
3. Electromyography:
  • Fibrillation potentials indicates Wallerian degeneration.
  • Polyphasic potentials indicate regeneration, and these are detected earlier than clinical recovery.
  • Volitional activity: indicated that the nerve is in continuity.

General management of facial paralysis

1. Reassurance of the patient.
2. Care of the eyes: To prevent exposure keratitis and corneal ulceration due to lack of Bell’s phenomenon (frequent blinking):
  • Artificial tears during the day.
  • Eye ointment by night.
  • Use of sun glasses outdoors.
  • In prolonged cases, lateral tarsorraphy or gold weight implantation.
3. Care of the paralyzed facial muscles: 
To prevent disuse atrophy and fibrosis:
a- Physiotherapy and gentle massage in a circular manner.
b- Infrared heat and galvanic stimulation.
c- When voluntary movement starts, the patient should start active exercises.

4. Treatment of facial paralysis according to the cause:

5- Rehabilitation
a- Dynamic: to improve the function of the nerve during movement provided there is good status of muscles.
- End to end anastmosis of the nerve.
- Nerve graft: The cable graft is obtained from the great auricular nerve in the neck, or from the sural nerve in the leg behind the lateral meleolus.
- Cross facial anastomosis: This is an anastomosis between the facial nerves of both sides, through a supralabial tunnel, using the sural nerve.
- Hypoglosso – facial anastmosis.
b- Static: to improve the appearance of the face at rest.
   - Implantation of fascia lata slings.
   - Regional muscle transplantation e.g. temporalis muscle in the cheek.

Results of facial paralysis

1- Contractures due to fibrosis of denervated muscles.
2- Tics and spasms.
3-Cross innervation due to misdirection of the regenerating fibers, resulting in:
A-Synkinesis. B-Crocodile tears: This is lacrimation while eating.

Important causes of facial paralysis

- Bell’s palsy. -Traumatic facial paralysis. - Herpes zoster oticus. -Active otitis media.

Causes of Facial nerve paralysis, aetiology

Here is the aetiology of facial nerve palsy.

I- Supra nuclear causes (Upper Motor Neuron Lesion [UMNL]):

  • Trauma to head.
  • Meningitis, encephalitis, and abscess.
  • Brain tumors.
  • Stroke: Hge, thrombosis, embolism.

II- Peripheral causes (Lower Motor Neuron Lesion [LMNL]):

(A) Intracranial:

1) In pons: Congenital nuclear aplasia, Basal meningitis, Pontine Haemorrage, Pontine tumors, Multiple sclerosis.
2) In CPA: Congenital cholesteatoma, Meningioma, Vestibular schwannoma.

(B) Cranial (intratemporal)

1) Traumatic:
  • Birth trauma: forceps delivery.
  • Fracture especially transverse type.
  • Surgical: mastoidectomy, stapedectomy.
2) Inflammatory:
3) Neoplastic:
4) IdiopathicBell’s palsy 
The commonest cause.

(C) Extra cranial

  1. Trauma: cut wound in parotid or face surgery.
  2. Sarcoidosis of the parotid.
  3. Tumor: malignant parotid tumors

(D) Miscellaneous

  • Polyneuritis (Guillane – Barre Syndrome).
  • Diabetes mellitus.
  • Lyme disease.
  • T.B.
  • Milkersson Rosenthal Syndrome.

Jul 10, 2018

Facial nerve anatomy, course and branches

(A) Intracranial part

Facial nerve has 3 nuclei:
  1. Motor nucleus lies in pons.
  2. Superior salivatory nucleus: in pons, parasympathetic secretomotor to lacrimal, submandibular, and sublingual glands.
  3. Nucles solitarius: in medulla, sensory, carries taste sensation from the tongue.
Motor fibers form the motor root, while parasympathetic and sensory fibers join to form the sensory root (nervus intermedius).

The 2 roots emerge on the side of the brain stem, at junction between pons & medulla to cross CPA to I.A.M. Controlled by pyramidal & extrapyramidal fibers.

(B) Cranial (intratemporal) part: 


  1. Labyrinthine segment: runs in the I.A.C superior to VIII & anterior to superior vestibular nerve, runs laterally to medial wall at geniculate ganglion.
  2. Tympanic (horizontal) segment: starts at geniculate ganglion, curves to form 1st genu, runs backwards in medial wall till the posterior wall.
  3. Mastoid (vertical) segment: Runs inferiority (2nd genu), lies antero inferior to lat. SCC, then vertically downwards to leave skull at stylomastoid foramen.

(C) Extra cranial part:

Enters parotid gland >> divides into terminal motor branches.

Branches of Facial nerve

(1) In temporal bone.

a) Greater superficial petrosal: arises at geniculate ganglion >> secreto motor parasympathetic to lacrimal, nasal, palatine glands.

b) Nerve to stapedius: motor supply to stapedius.

c) Chorda tympani: exit just above stylomastoid foramen to enter ME >> carries taste from ant. 2/3 of tongue & secretomotor parasympathetic to sub lingual and sub mandibular glands.

(2) After exit from skull:

Two motor branches to stylohyoid & post belly of digastric.
Posterior auricular nerve: motor to occipital belly of occipitofrontalis.

(3) Five terminal branches in parotid:

Temporal, zygomatic, buccal, mandibular & cervical supply muscles of scalp, face, auricles & platysma.