IPHREHAB : OSTEOMALACIA & RICKETS WITH TREATMENT

IPHREHAB


OSTEOMALACIA & RICKETS

DEFINITION
It is a condition characterised  by defective bone mineralisation.
There is increased bone turnover.
It is usually due to Calcium & Vitamin D deficiency.
Condition is rare in USA, UK..
More common in Arab countries

DEFINITION

Rickets is seen in children before Puberty..

Osteomalacia is adult counterpart of Rickets..

Both have same aetiology :

There is failure or defective mineralisation of newly formed matrix

AETIOLOGY

Diet poor in calcium & Vitamin D

Malabsorption Syndromes Chronic Diarrhoea, Sprue,    Steatorrohoea, 

Tuberculosis of Intestines

Chronic  Renal Failure  

AETIOLOGY

Lack of Sunlight Exposure- Reduced Vit. D Conversion 

Hypophophatemia

Vitamin D Resistance Rickets

There is increased thickness of Osteoid Seams, reduces calcification –mineralisation is defective

VITAMIN D METABOLISM

Ultraviolet Rays 

Skin 7-DHC (dehydrocholesterol)

Vitamin D3

Liver  - converts into 25-hydroxylase

Inactive 25(OH) D3

Kidney- 25(OH) Vitamin D 1-a hydroylase

Biological Active 1,25 (OH)2 D3  

Increases absorption of calcium from gut

CLINICAL PICTURE

Delayed DEVELOPMENT-Short Stature

Decreased Muscular Tone (Hypotonia)

Craniotabes  6-12 years 

Frontal Bossing

Delayed Frontallae Closing

Enlargement of Epiphysis (Rickets Rosary)

CLINICAL PICTURE

Teeth are pitted Caries common

Pot-belly Abdomen

Carpopedal Spasms

Laryngeal Stridor

Tetany may be seen

Bone Pains – Defective spine

Waddling Gait

INVESTIGATIONS

Complete Blood Anaemia Common

Serum Calcium Low

Phosphates usually low 

Alkaline Phosphatase raised

X-ray of bones characterstic changes in children Epiphysis thined & distal end of bone widened SAUCER deformity

INVESTIGATIONS

In Adults bone X-ray may be normal or shows osteoporosis

In Children Pseudofractures & Looser’s zones (Radiolucent bands)  may be seen It affects the ribs, Axilliary border of Scapula, Pubic rami

X-Ray of Rickets

BOWED  LEGS

MANAGEMENT

Calcium 1-2 gm daily

Diet- 1 litre of milk

Vitamin D 60,000 IU (1.5 mg of D3) Daily Orally

For tetany IV Calcium gluconate is given

Response to treatment is excellent

Conservative Management

1.Dietary supplement:

2.Physiotherapy treatment :

 .Gentle range of motion exercise.

 .Gradual weaght bearing training.

 .Prevention from fall and injury.

 .Coordination and reconditioning.

 .Light endurance training.

IPHREHAB : INFECTION, TYPHOID

IPHREHAB

TYPHOID

• Very common disease in our country
• Outbreaks are known to occur from time to time
• Pollution & Insanitary condition
• Present in animals except S.Typhi
• Transmitted by food, water, Milk
•  May be directly from one person to another

AETIOLOGY

• Caused by Salmonella Group of Organisms
• Reservoir are animals except for S.Typhi which is seen only in human beings
• There are 2000 Serotypes
• Faeco-oral route
• Tranmission through food, Flies & Fomites
• It involves Payer’s patches of small Intestines

CLINICAL PICTURE

• Fever is most common presenting symptom
• Fever is step ladder pattern
• Onset is insidious
• There is Malaise, Headache, Cough,  Drowsiness & Bodyaches
• Constipation common
• Relative Bradycardia
• Rash may appear on fifth day
• Toxaemia is Max. in 2nd Week
• Spleen is palpable
• Toxaemia increases in 3rd Week
• Coma may set in & may lead to death
• Antibiotics give the best results
• Carriers are well known

INVESTIGATIONS

• Complete Blood Leukopenia Increase in Lympho
• Blood Culture +ve  first week
• Widal’s  Test  2nd Week Rising titer is diagnostic
• Urine & Stool Culture

COMPLICATIONS

• Perforation
• Haemorrhage
• Osteomyelitis
• Meningitis
• Myocarditis
• Pneumonia
• Nephritis
• Hepatitis

MANAGEMENT

• General Management :- Analgesics for fever, Antiemetics (Perinorm) for vomiting
• Antibiotics Ciproflxacillin 500mg BD
• Cotrimoxazole 
• Amoxycillin
• Carrier Ciproflox for 4 weeks
• Prevention - Vaccination

IPHREHAB : INFECTIONS, MEASLES AND MUMPS

IPHREHAB

INFECTIONS

MEASLES

• It is caused by Virus ( Paramyxo)
• It is usually seen in children
• One attack give permanent immunity
• It is in in severe form in malnourished person ( in our country)
• Very high mortality
• Incubation period is 10 days

CLINICAL  PICTURE

• Catarrhal Stage    High Fevere    Severe Nasal Catarrh Sneezing, Redness of Eyes- Conjuctivitis Kapolick Spots in mouth
• Cough Hoareseness of Voice Photophobia
• Child is very irritable & in Miserable Stage
• Exanthematous stage  Koplik  spots disappear  Rash appear on 2-4 day  Rash is maculo papular initially on back of   ear
• It rapidly spread over the body – become blotchy
• Rash settle down in one week Fever subside

COMPLICATIONS

• Stomatitis Entertitis Pneumonia Keratitis
• Otitis Media, Conjunctivitis
• Brochopneumonia
• Encephalitis
• Malnutrition Vitamin A deficiecy
• Severe weight loss

MANAGEMENT

• Bed Rest No schooling for 10 days
• Symptomatic Treatment
• Antibiotics
• Prevetion – active immunisation
• Passive immunisation in serious cases  250 mg IM

MUMPS

• Common disorder in our country
• Caused by virus
• Incubation period 18 days
• Spread by droplet infection
• Not very virulent
• Infectivity ver low
• May remain subclinical

CLINICAL  PICTURE

• Fever
• Pain in the jaw
• Trismus
• Swelling of Parotid Gland subside in 2-3 days
• Meningitis Encephalitis
• Pancreatitis
• Orchitis

MANAGEMENT

• Treat the symptoms
• Antibiotics if bact. Infection is present
• In orchitis cases give predisolone 40 mg daily
• Vaccination for prevention- MMR

IPHREHAB : INFECTIONS, DIPHTHERIA

IPHREHAB

INFECTIONS

DIPHTHERIA

• It is disease caused by Gram + Bacteria
• Bacteria produces Exotoxin – which damages Heart & Nervous system
• It is common in India usually affecting children
• Sore Throat is presenting symptom
• Disease spread by droplet Infection

CLINICAL PICTURE

• Incubation period is 2-4 days
• Infection can occur over the Conjunctiva, Genital tract, Wounds & Abrasions
• Fever is high
• Grayish Green Membrane on Tonsils
• Membrane is firm & adherent
• Swelling of Neck (Bull’s Neck)
• Nasal Infection Common 
• Nasal Discharge ++ – May be Bloody in nature
• Husky voice due to Laryngitis
• Respiratory Infection can lead to death
• ECG may show tachycardia & T-wave changes
• Palatal Paralysis
• Accommodation may be paralysed
• Polyneuritis is seen in few cases

MANAGEMENT

• Inform the Public Health Department
• Give anti-toxin 4000-32000 IM
• Benzyl Penicillin -4 lacs Units 6 hourly for one week
• Treat Complications -  Resp. & Cadiac
• Protect Close relatives Erythromycin Immunization.

IPHREHAB : DEEP VEIN THROMBOSIS

IPHREHAB

DEEP VEIN THROMBOSIS

DEFINITION

It is characterized by formation of clots in deep veins of body

It is more common in lower limbs and thighs

It is dangerous condition- clot can detach and lead to pulmonary embolism

Early detection is must to prevent this complication 

PREVELANCE : 

• IT IS VERY COMMON CONDITION
• SECOND MOST COMMON CAUSE  OF VASCULAR PROBLEM
• IN USA  600,000 CASES ARE DIAGNOSED EVERY YEAR
• ONE IN 100 DIES OF PULMONARY EMBOLISM
• IT IS COMMON AFTER 60 YEARS

PERSONS AT RISK

• THE ELDERLY
• DIABETICS
• HAVING BLOOD DISEASES
• WOMEN ON ORAL CONTRACEPTIVES-Oesterogens
• HISTORY OF PREVIOUS THROMBOSIS
• MAJOR SURGERY

• HOSPITALIZED PATIENTS
• PERSONS ON PROLONGED BED REST (Persons confined to bed)
• IMMOBILISED PERSONS –Fracture Neck femur
• PASSENGERS ON LONG INTERNATIONAL FLIGHTS-(Economy Class Syndrome

PERSONS AT RISK

• PARALYSED CASES
• CANCER PATIENTS
• PREGNANCY & CHILD BIRTH
• CONGESTIVE FAILURE
• CIRCULATORY PROBLEMS

DEEP VEIN THROMBOSIS

CLINICAL PICTURE

Symptoms

1. Discoloration of the legs 
2. Calf or leg pain or tenderness 
3. Swelling or Oedema of the legs or both feet lo 
4. Warm skin 
5. Surface veins become more visible 
6. Leg fatigue
7. Pain worst on standing 

SIGNS

• PALPABLE THROMBOSED VEINS
• CALF TENDERNESS
• ECCHYMOSIS
• LIMBS ARE WARM
• CONSTITUTINAL SYMPTOMS
• PULMONARY EMBOLISM

Flight-related Deep Vein Thrombosis (DVT) 

• AN IMPORTANT ENTITY
• KNOWN AS “ECONOMY CLASS SUNDROME”
• SEEN IN PERSONS ON LONG DISTANCE TRAVEL
• OBESE,, OEDEMATOUS
• DEHYDRATED
• COAGULATION DISORDERS

MANAGEMENT  :

Preventive

• PHYSIOTHERAPY VERY EFFECTIVE
• STAND UP & WALK
• CALF MUSCLE EXERCISES
• LOT OF FLUIDS
• NO ALCOHOL
• NO SMOKING
• AVOID CROSS LEGS IN POSTURE
• WEAR LOOSE CLOTHING

MANAGEMENT

• REDUCE WEIGHT
• ELEVATE YOUR LEGS
• STOCKINGS
• ROLE OF ASPIRIN
• LOW DOSE HEPARIN
• WARFARIN

IPHREHAB: Spontaneous Subarachnoid Hemorrhage

IPHREHAB

Spontaneous Subarachnoid Hemorrhage

This is the fourth most frequent cerebrovascular disorder following atherothrombosis, embolism, and primary intracerebral hemorrhage. Saccular aneurysms are also called berry” aneurysms; actually they take the form of small, thin-walled blisters protruding from arteries of the circle of Willis or its major branches. Their rupture causes a flooding of the subarachnoid space with blood under high pressure.

Aneurysms are multiple in 20 percent of patients

In childhood , rupture of saccular aneurysms is rare, and they are seldom found at routine postmortem examination; beyond childhood, they gradually increase in frequency to reach their peak incidence between 35 and 65 years of age.

Approximately 90 to 95 percent of saccular aneurysms lie on the anterior part of the circle of Willis.

Clinical picture

• Prior to rupture, saccular aneurysms are usually asymptomatic. Exceptionally, if sufficiently large to compress pain-sensitive structures, they may cause localized cranial pain.
• The presence of a partial oculomotor palsy with dilated pupil may be indicative of an aneurysm of the posterior communicating-- internal carotid junction.
• With rupture of the aneurysm, blood under high pressure is forced into the subarachnoid space(where the circle of Willis lies).
• Rupture of the aneurysm usually occurs while the patient is active rather than during sleep , and in some instances sexual intercourse, straining at stool, lifting heavy objects, or other sustaining exertion precipitates the ictus. In patients who survive the initial rupture, the most feared complication is rerupture, an event that may occur at any time from minutes up to 2 or 3 weeks later.
• In less severe cases, consciousness, if lost , may be regained within a few minutes or hours, but a residual of drowsiness, confusion, and amnesia accompanied by  severe headache and stiff neck persists for several days.
• Since the hemorrhage is confined to the subarachnoid space, there are few or no focal neurologic signs.
• AVM is another most common cause for SAH
• Convulsive seizures, usually brief and generalized.

• Vasospasm  Delayed hemiplegia or other focal deficit usually appears 3 to 12 days after rupture and rarely before or after this period. These delayed accidents and the focal narrowing of a large artery or arteries, seen on angiography, are refered to as vasospasm.
• Hydrocephalus  If a large amount of blood ruptures into the ventricular system or floods the basal subarachnoid space, The patient then may become confused or unconscious as a result of acute hydrocephalus. A subacute hydrocephalus due to blockage of the CSF pathways by blood may appear after 2 to 4 weeks.

Laboratory Findings  

A CT scan will detect blood locally or diffusely in the subarachnoid spaces or within the brain or ventricular system in more than 90 percent of cases and in practically all cases in which the hemorrhage has been severe enough to cause momentary or persistent loss of consciousness.

In all other cases a lumbar puncture should be undertaken when the clinical features suggest a subarachnoid hemorrhage. Usually the CSF is grossly bloody within 30 min of the hemorrhage, with RBC counts up to 1 million per cubic millimeter or even higher.

Carotid and vertebral angiography is the only certain means of demonstrating an aneurysm and does so in some 85 percent of patients in whom the correct diagnosis of spontaneous subarachnoid hemorrhage is made on clinical grounds.

MRI and MRA detect most aneurysms of the basal vessels but are as yet of insufficient sensitivity to replace conventional angiography. Even when MRA or “ CT angiography  “ demonstrates the aneurysm, the surgeon usually requires the kind of anatomic definition that can only be obtained by conventional angiography. 

Establish the diagnosis

If there is a typical history, marked neck stiffness and no focal neurological deficit, lumbar puncture is still the best way to make the diagnosis, revealing uniformly blood-stained CSF. 

If the history is typical with marked neck stiffness, but the patient remains in coma or shows a marked focal neurological deficit, a CT scan is a safer way to establish the diagnosis (revealing blood in the subarachnoid space),since lumbar puncture may lead to worse condition in this group of patients (whose coma or focal neurological deficit may indicate the presence of an associated intracerebral blood clot).

Treatment 

• This is influenced by the neurologic and general medical state of the patient as well as by the location and morphology of the aneurysm.
• The general medical management in the acute stage includes the following , in all or part: 
• bed rest
• fluid administration to maintain above-normal circulating volume and central venous – pressure
• use of elastic stockings and stool softeners
• administration of beta-blockers
• calcium channel blockers

Treatment 

• intravenous nitroprusside
• or other medication to reduce greatly elevated blood  pressure and then maintain systolic blood pressure at 150 mmHg or less;
• and pain-relieving medication for headache ( this alone will often reduce the hypertension ).
• The prevention of systemic venous thrombosis is critical, usually accomplished by the use of cyclically inflated whole-leg compression boots.

Treatment 

• The use of anticonvulsants is controversial; many neurosurgeons administer them early, with a view of preventing a seizure-induced risk of rebleeding.
• Calcium channel blockers are being used extensively to reduce the incidence of stroke from vasospasm. Nimodipine 50 mg, administered intravenus, is currently favored.
• Notable advances in the techniques for the obliteration of aneurysms, particularly the operating microscope, and the management of circulatory volume have significantly improved the outcome of patients with ruptured aneurysms.
• Both the risk of rerupture of the aneurysm and some of the secondary problems that arise because of the massive amount of blood in the subarachnoid space can be obviated by early obliteration of the aneurysm.
• lumbar puncture is carried out for diagnostic purposes if the CT scan is inconclusive; thereafter this procedure is performed only for the relief of intractable headache, to detect recurrence of bleeding, or to measure the intracranial pressure prior to surgery. 
• Advice from specialist neurosurgical units should be sought. Patients who have withstood their first bleed well are submitted to carotid and vertebral angiography within a few days to establish whether or not an operable aneurysm is present. Patients who do not recover from their first bleed well, patients with inoperable aneurysms should be nursed in bed for a few weeks and then mobilized over a further few weeks, being encouraged to return to full normal activities at about 3-4 months.
• Prevent re-bleeding

Rehabilition

Since the incidence of significant damage to the brain is high  in patients surviving subarachnoid haemorrhage, many will not be able to return to normal activities.

They will need support from relatives,  nurses, physiotherapists, speech therapists, occupational therapists, social workers and specialist units in rehabilitation.

Course and prognosis

 Patients with the typical clinical picture of spontaneous subarachnoid hemorrhage in whom an aneurysm or arteriorvenous malformation cannot be demonstrated angiographically have a distinctly better prognosis than those in whom the  lesion is visualized.

 Vasospasm and rebleeding were the leasing causes of morbidity and mortality in addition to the initial bleed. In respect to rebleeding , Aoyagi and Hayakawa found that this occurred within 2 weeks in 20 percent of patients, with a peak incidence in the 24 h after the initial bleed.

IPHREHAB : Intracranial Hemorrhage

IPHREHAB

Intracranial Hemorrhage
This is the common, well-known “spontaneous” brain hemorrhage. It is due predominantly to chronic hypertension and degenerative changes in cerebral arteries.Hemorrhage may interfere with cerebral function through a variety of mechanisms, including destruction or compression of brain tissue and compression of vascular structures, leading to secondary ischaemia and edema.
Intracranial hemorrhage is classified by its location as intracerebral, subarachnoid, subdural, or epidural, all of which- except subdural hemorrhage- are usually  caused by arterial bleeding.


The bleeding occurs within brain tissue, and rupture of arteries lying in the subarachnoid space is practically unknown apart from aneurysms. The extravasation forms a roughly circular or oval mass that disrupts the tissue and grows in volume as the bleeding continues . Adjacent brain tissue is distorted and compressed. If the hemorrhage is large, midline structures are displaced to the opposite side and reticular activating and respiratory centers are compromised, leading to coma and death.

1. Intracerebral Hemorrhage

Of all the cerebrovascular diseases, brain hemorrhage is the most dramatic.It has been given its own name, “apoplexy”.

Clinical Picture

• With smaller hemorrhages, the clinical picture conforms more closely to the usual temporal profile of a stroke, i.e, an abrupt onset of symptoms that evolve gradually and steadily over minutes, hours, or a day or two, depending on the size of the ruptured artery and the speed of bleeding. 
• Headache and vomiting are cardinal features.Very small hemorrhages in “silent” regions of the brain may escape clinical detection.
• Clinical features vary with the site of hemorrhage.
• Deep cerebral hemorrhage  The two most common sites of hypertensive hemorrhage are the putamen and the thalamus, which are separated by the posterior limb of the internal capsule. This segment of the internal capsule is traversed by descending motor fibers and ascending sensory fibers, including the optic radiations.
• Lobar hemorrhage  Hypertensive hemorrhages also occur in subcortical white matter underlying the frontal, parietal, temporal, and occipital lobes. Symptoms and signs vary according to the location.
• Pontine hemorrhage  With bleeding into the pons, coma occurs within seconds to minutes and usually leads to death within 48 hours. Ocular findings typically include pinpoint pupils. Horizontal eye movements are absent or impaired, but vertical eye movements may be preserved.
• Cerebellar hemorrhage  The distinctive symptoms of cerebellar hemorrhage (headache, dizziness, vomiting, and the inability to stand or walk) begin suddenly, within minutes after onset of bleeding.

Laboratory Findings  

Among laboratory methods for the diagnosis of intracerebral hemorrhage, the CT scan occupies the foremost position. In CT scans, fresh blood is visualized as a white mass as soon as it is shed. The mass effect and the surrounding extruded serum and edema are hypodense.

By MRI, either in T1-or-T2 weighted images, the hemorrhage is not easily visible in the 2 or 3 days after bleeding.

In general, lumbar puncture is ill advised, for it may precipitate or aggravate an impending shift of central structures and herniation. The white cell count in the peripheral blood may rise transiently to 15,000 per cubic millimeter, a higher figure than in thrombosis.

Differential Diagnosis: 

Putaminal, thalamic, and lobar hypertensive hemorrhages may be difficult to distinguish from cerebral infarctions. To some extent, the presence of severe headache, nausea and vomiting, and impairment of consciousness are useful clues that a hemorrhage may have occurred; the CT scan  identifies the underlying disorder definitively.

CT scan or MRI is the most useful diagnostic procedure, since hematomas can be quickly and accurately localized.

IPHREHAB : Transient Ischemic Attacks(TIA) & CEREBRAL THROMBOSIS

IPHREHAB

1.Transient Ischemic Attacks(TIA)
Current opinion holds that TIAs are brief, reversible episodes of focal, nonconvulsive ischaemic neurologic disturbance, Consensus has been that their duration should be less than 24 h.

Clinical picture
Transient Ischaemic Attacks can reflect the involvement of any cerebral artery. The loss of function entirely depends on the influenced artery. It may last  a  few seconds or up to 12 to 24 h, Most of them last 2 to 15 min. There are only a few attacks or several hundred. Between attacks, the neurologic examination may disclose no abnormalities. A stroke may occur after numerous attacks have occurred over a period of weeks or months.

Differential diagnosis of TIAs

Transient episodes, indistinguishable from TIAs, are known to occur in patients with Seizure,Migraine,Transient global amnesia,and occasionally in patients with multiple sclerosis, meningioma, glioblastoma ,metastatic brain tumors situated in or near the cortex ,and even with subdural hematoma.

2. Cerebral thrombosis

Most cerebrovascular disease can be attributed to atheroscleroses and chronic hypertension; until ways are found to prevent or control them, vascular disease of the brain will continue to be a major cause of morbidity.

Pathogenesis

Pathogenesis of Ischemic neuronal death

   Ischemia

       ↓ 

   Excitatory amino acid receptors

       ↓ 

   Borderzone or penumbra    ↓

   Programmed cell death

Clinical picture  

In general, evolution of the clinical phenomena in relation to cerebral thrombosis is more variable than that of embolism and hemorrhage. The loss of function that the patient notices, and which may be apparent on examination, entirely depends on the area of brain tissue involved in the ischaemic process.

Clinical picture

In more than half of  patients, the main part of the stroke is preceded by minor signs or one or more transient attacks of focal neurologic dysfunction. The final stroke may be preceded by one or two attacks or a hundred or more brief TIAs, and stroke may follow the onset of the attacks by hours, weeks, or, rarely, months.

The most occurrence of the thrombotic stroke is during sleep.The patient awakens paralyzed. Either during the night or in the morning.

Unaware of any difficulty, he may arise and fall helplessly to the floor with the first step.

Clinical picture

Associated symptoms

Seizures accompany the onset of stroke in a small number of cases (10-50%); in other instances, they follow the stroke by weeks to years. The presence of seizures does not definitively distinguish embolic from thrombotic strokes, but seizure at the onset of  stroke may be more common with embolus.

Headache  occurs in about 25% of patients with ischaemic stroke, possibly because of the acute dilation of collateral vessels.

Laboratory Findings

• CT Scan or MRI: A CT scan or MRI  should be obtained routinely to distinguish between infarction and hemorrhage as the cause of stroke, to exclude other lesions (eg, tumor, abscess) that can mimic stroke, and to localize the lesion. CT is usually preferred for initial diagnosis because it is widely available and rapid and can readily make the critical distinction between ischaemia and hemorrhage.
• Lumbar Puncture: This should be performed in selected cases to exclude subarachnoid hemorrhage.
• Cerebral Angiography: Intra-arterial angiography is used to identify operable extracranial carotid lesions in patients with anterior circulation TIAs who are good surgical candidates. It also can be used for intra-arterial thrombolysis ( r-tPA)
• Magnetic resonance  Angiography (MRA) may detect stenosis of large cerebral arteries, aneurysms, and other vascular lesion, but its sensitivity is generally inferior to that of conventional angiography.