Patient Can Be Compensated If Discharge Card Is Incomplete

Documentationisan important aspect of medical care.It is important to document whatever you say in the form of instructions on the discharge card or prescription order and also ensure that the patient/relative comprehends the same

Medical record documentation is an important part of the treatment of the patient. In a recent judgement consumer court has made it clear that if patient’s discharge card carry inadequate instruction, the patient can be compensated for that.c

The case involved was decided in Kumari Laxmi Vs Dr S K Govil and Ors in Madhya Pradesh State Consumer Dispute Redressal Commission> After the treatment the patient required to comme back after 3 days but doctors did not give this in writing on discharge card.

Patient came after three weeks and had some problems for which the court held the doctors responsible.

The Mastoid and Its Air Cell System

The mastoid consists of a cortex of bone with a “honeycomb” of air cells underneath. Depending on air cell development three types of mastoid have been described.

  1. Well-pneumatised or cellular. Mastoid cells are well developed and the intervening septa are thin.
  2. Diploetic. Mastoid consists of marrow spaces and a few air cells.
  3. Sclerotic or acellular: There are no cells or marrow spaces.

With any types of pneumatisation, antrum is always present. In sclerotic mastoids the antrum is usually small and sigmoid sinus anteposed.

Depending on the location, mastoid air cells are divided into:

  1. Zygomatic cells (in the root of zygoma)
  2. Tegmen cells (extending in tegmen tympani)
  3. Perisinus cells (overlying the sinus plate)
  4. Retrofacial cells (round the facial nerve)
  5. Perilabyrinthine cells (located above, below and behind the labyrinth, some of them passing through the arch of superior semicircular canal. These cells may communicate with the petrous apex)
  6. Peritubal (around the Eustachian tube. Along with hypotympanic cells they also communicate with the petrous apex)
  7. Tip cells which are quite large and lie medial and lateral to the digastric ridge in the tip of mastoid
  8. Marginal cells (lying behing the sinus plate and may extend into the occipital bone)
  9. Squamosal cells (lying in the squamous part of temporal bones).

Ascesses may form in relation to these air cells and may sometimes be far removed from the mastoid region.

Development of Mastoid

Mastoid develops from the squamousp and petrous bones. The petrosquamosal suture may persist as a bony plate the Korner’s septum, separating superficial squamosal cells from the deep petrosal cells. Korner’s septum is surgically important as it may cause difficulty in locating the antrum and the deeper cells, and thus lead to incomplete removal of disease at mastoidectomy.

Text adapted from Diseases Of Ear, Nose and Throat by PL Dhingra, 2nd Edition

The Middle Ear

The middle ear together with the Eustachian tube, aduts, antrum and mastoid air cells is called the middle ear cleft. It is lined by mucous membrane and filled with air.

The middle ear extends much beyond the limits of tympanic membrane which forms its lateral boundary and is sometimes divided into

  1. mesotympanum (lying opposite the pars tensa)
  2. epitympanum or the attic (lying above the pars tensa but medial to Shrapnell’s membrane and the bony lateral attic wall)
  3. hypotympanum (lying above the level of pars tensa). The portion of middle ear around the tympanic orifice of the Eustachian tube is sometimes called the protympanum.

Middle ear can be likened to a six-sided box with a roof, a floor, medial, lateral, anterior and posterior walls.

The roof is formed by a thin plate of bone called tegmen tympani. It also extends posteriorly to form the roof of the aditus and antrum. It separates tympanic cavity from the middle cranial fossa.

The floor is also a thin plate of bone which separates tympanic cavity from the jugular bulb. Sometimes it is congenitally deficient and the jugular bulb may then project into the middle ear, separated from the cavity by the mucosa only.

The anterior wall has a thin plate of bone which separates the cavity from internal carotid artery. Ti also has two openings; the lower one for the Eustachian tube and the upper one for the canal of tensor tympani muscle.

The posterior wall lies close to the mastoid air cells. It presents a bony projection called pyramid through the summit of which appears the tendon of the stapedius muscle to get attachment to the neck of stapes. Aditus, an opening through which attic communicates with the antrum, lies above the pyramid. Facial nerve runs in the posterior wall just behind the pyramid.

Facial recess or the posterior sinus is a depression. In the posterior wall lateral to the pyramid. It is bounded medially by the vertical part of VIIth nerve, laterally by the chorda tympani and above by the fossa incudis. Surgically facial recess is important as direct access can be made through this into the middle ear without disturbing posterior meatal wall (intact canal wall technique).

The medial wall is formed by the labyrinth. It presents a bulge called promontory which is due to the basal coil of cochlea; oval window into which is fixed the footplate of stapes; round window or the fenestra cochleae which is covered by the secondary tympanic membrane.

Above the oval window is the canal for facial nerve. Its bony covering may sometimes be congenitally dehiscent and the nerve may lie exposed making it very vulnerable to injuries or infection. Above the canal for facial nerve is the prominence of lateral semicircular canal. Just anterior to the oval window, the medial wall presents a hook-like projection called the processus cochlear informis.

The tendon of tensor tympani takes a turn here to get attachment to the neck of malleus. The cochleariform process also marks the level of the genu of the facial nerve. Medial to the pyramid is a deep recess called sinus tympani which is bounded by the subiculum below and the ponticulus above.

The lateral wall is formed largely by the tympanic membrane and to a lesser extent by the bony outer attic wall called the scutum. The tympanic membrane is semitransparent and forms a “window” into the middle ear.

Mastoid Antrum

It is a large, air-containing space in the upper part of mastoid and communicates with the attic through the aditus. Its roof is formed by the tegmen antri which separates it from the middle cranial fossa. The lateral wall of antrum is formed by a plate of bone which is on an average 1.5 cm thick in the adult. It is marked externally, on the surface of mastoid by suprameatal (MacEwen’s) triangle.

Aditus and Antrum

Aditus is an opening through which the attic communicates with the antrum. The bony prominence of ht ehorizontal canal lies on its medial side while the fossa incudis, to which is attached the short process of incus, lies laterally. Facial nerve courses just below the aditus.

If The Day Is Busy Patients are Discharged Earlier

A new study done to examine the behavior of hospital admission and discharge behavior is affected by fluctuations in demand. It found that  that on days when hospitals have a  high demand, patients are discharged earlier than expected.when compared to those discharged on days when demand is low.

The study was conducted by the RAND Journal of Economics. Rajiv Sharma, Miron Stano, and Renu Gehring used Oregon hospital data to analyze the question of hospital constraint affecting the  admission  and discharge decisions.

A total of 380,000 records were used by the researchers.

The External Ear

Anatomy of Ear

Anatomy of Ear

The external ear consists of the (i) auricle or pinna, (ii) external acoustic meatus and (iii) the tympanic membrane.

1. Auricle or Pinna

The entire pinna, except its lobule, and the outer part of external acoustic meatus is made up of a framework of a single piece of yellow elastic cartilage covered with skin.

The latter is closely adherent to te perichondrium on its lateral surface while it is slightly loose on the medial surface. The various elevations and depressions seen on the lateral surface of pinna.

There is no cartilage between the tragus and crus of the helix. An incision made in this area will not cut through the cartilage and is used for endaural approach in surgery of the meatus or mastoid. Pinna is also the source of several graft materials for the surgeon.

Cartilage from the tragus, perichondrium from the tragus or concha and fat from the lobule are frequently used for reconstructive surgery of the middle ear.

The conchal cartilage has also been used to correct depressed nasal bridge while the composite grafts of the skin and cartilage from the pinna are sometimes used for repair of defects of nasal ala.

2. External Acoustic (Auditory) Meatus

It extends from the bottom of the concha to the tympanic membrane and measures about 24 mm along its posterior wall. The meatus is not a straight tube, its outer part is directed upwards, backwards and medially while its inner part is directed downwards, forwards and medially. Therefore, to see the tympanic membrane, the pinna has to be pulled upwards, backwards and laterally so as to bring the two parts in alignment.

The meatus is divided into two parts: [Read more...]

Making A Diagnosis In Patient of Edema

Congestive Cardiac Failure

  • The edema is found on the most dependent parts of the body as gravity plays an important part.
  • In an ambulatory patient edema is in the feet, ankles and legs
  • In the recumbent patient it is mainly over the sacrum, lumbar region and genitalia.
  • Edema is most marked in the evening.

Left ventricular failure

Here accumulation of fluid in the lung comes much earlier than edema of the feet, resulting in

  • Dyspnea
  • Cough
  • Basal rales.

Pericardial effusion

Here since there is obstruction to the flow of blood into the right atrium, edema of feet may occur, but no edema of lungs occurs because the heart is able to pump the little blood it receives into the lungs and general circulation. It is associated with raised JVP, hepatomegaly and ascites.

Acute nephritis

  • Edema is generalized and not restricted to the dependent parts of the body.
  • It is more noticeable in the early morning.
  • The fluid accumulates initially in the loose connective tissues, hence it is most marked around the eyelids and face.
  • The cause of edema is damage to the endothelial lining of the capillaries, disturbance of fluid and sodium excretion and later also due to hypoproteinemia.

Nephrosis

The swelling is generalized and massive due to hypoproteinemia following massive albuminuria.

Hepatic (Portal hypertension):

Here ascites occurs before edema of feet. This occurs due to hypoproteinemia and compression of the hepatic branches of the portal vein. Ascites leads to pressure on the venous circulation in the lower limbs leading to edema of the legs.

Inferior vena cava obstruction

This is characterized by bilateral nondependent painless pitting edema. Collateral dilated veins are usually present in the flanks with flow of blood from below upwards.

Myxedema

Here edema is non-pitting, associated with puffy face, weight gain, weakness, alopecia, hoarse voice, rough dry skin, constipation, anemia and menstrual disturbances.

6. Allergic (Angioneurotic edema):

This often resembles myxedema with swelling over the face and limbs. There is usually intense itching and bronchospasm.

7. Nutritional:

This is characterized by dependent edema with puffiness of face, pallor and cachexia.

8. Filariasis:

In filariasis, edema occurs due to destruction of the lymphatic filter action of the lymph glands with consequent blocking and dilation of the lymph vessels. Subsequently there is transudation of lymph, rich in proteins, into the tissues. Later connective tissues proliferate leading to elephantiasis. This is characterized by unilateral non-pitting edema with rough skin. There may be history of fever with rigors especially at night and initially pitting edema. Blood smear may show microfilaria.

9. Gout:

This commonly affects the big toe with marked pain, edema and deformity of the part involved. Tophi may be present. There may be history of renal colic or renal stones.

10. Venous Thrombosis:

This is characterized by unilateral painful pitting edema.

Callosity

Callosity

Callosity is a superficial, circumscribed yellowish white flat thickened patch of hyperkeratotic material. It is a localized thickened part of the skin. Microscopically, there is thickening of the epidermis particularly the stratum corneum and the granular layer, the rete pegs are atrophic.

Clinical it is a localized thickened area of skin which has no central core as seen in a corn. The lesion is a diffuse thickening. Callosity is particularly seen at the regions of pressure or friction particularly in the hands and feet. It is often seen in a gardener’s hand. Callosity is a painless condition.

No particular treatment is required. The patient however takes the help of a chiropodist for paring of this lesion.

What Is Edema -How and Why Does It Occur?

Edema is the collection of fluid in the interstitial spaces or serous cavities. It becomes evident only when 5-6 liters of fluid has accumulated in the water depots.

Pitting on pressure occurs when the circumference of the limb is increased by 10%.

Mechanism : One or more of the following factors may be responsible.

  • Increased capillary permeability when it is damaged e.g. acute inflammation.
  • Increased capillary pressure e.g. cardiac failure.
  • Decreased osmotic pressure of the blood e.g. hypoproteinemia.
  • Damaged lymphatic drainage e.g. filariasis.

Site

Venous edema commonly occurs in the lower limbs which are most dependent. However, if the patient is recumbent (i.e. lies on his back), edema may be present only over the sacral region which is, then, most dependent. Lymphatic edema may occur in either limbs or over scrotum depending upon the site of involvement.

Causes

Bilateral Edema:

  1. Cardiac: CCF, LVF, pericarditis
  2. Renal: Acute nephritis, nephrosis
  3. Hepatic: Cirrhosis of liver, portal hypertension
  4. Venous: Inferior vena cava obstruction
  5. Endocrine: Myxedema
  6. Allergic: Angionurotic edema
  7. Nutritional: Anemia, hypoproteinemia, beriberi.
  8. Toxic: Epidemic dropsy

Unilateral:

A. Lymphatic:

  1. Filarial
  2. Pressure by new growth, metastasis
  3. Radiation

B. Traumatic: Bruises, sprains, fractures
C. Infections: Cellulitis, boils, carbuncle
D. Metabolic: Gout
E. Venous: Venous thrombosis, varicose vains.
F. Hereditary: Milroy’s disease

Corn

It is a localized hyperkeratosis of the skin. Histologically a corn is composed of keratin masses with intact basal layer.

It usually occurs at the sites of pressure e.g. on the sole, foot and toes. This occurs often due to ill fitting or tight shoes. There is usually a horny induration of the cuticle with a hard centre.

A corn is a circumscribed, horny thickening, which is cone-like in shape with apex pointing inward and base towards the surface. Corn may be painful particularly when it is rubbed. Corn has a tendency to recur after excision. A corn has a deep central core which reaches the deper layers of dermis.

Corn is very painful.

Treatment

    • Corns may spontaneously disappear when the causative factor is removed.
    • Salicylic acid in collodion on successive nights may be applied.
    • Central local applications have been effective such as Corn cap.
    • If these measures fail and the corn is painful, it should be excised with particular care to take off the deep root of the central core. This prevents recurrence.

    Prevention

    • Use of good footwear
    • Soft shoes or soft pads at the pressure points of the sole.

    Digital Clubbing and Its Causes

    Clubbing is bulbous enlargement of soft parts of the terminal phalanges with both transverse and longitudinal curving of the nails. The swelling of the terminal phalanges in clubbing occurs due to interstitial edema and dilation of the arterioles and capillaries.
    Clubbing develops in five steps:

    1. Fluctuation and softening of the nail bed (increased ballotability)
    2. Loss of the normal <165° angle (“Lovibond angle”) between the nailbed and the fold (cuticula)
    3. Increased convexity of the nail fold
    4. Thickening of the whole distal (end part of the) finger (resembling a drumstick)
    5. Shiny aspect and striation of the nail and skin

    Causes of Clubbing

    Pulmonary

    • Bronchogenic carcinoma
    • Lung abscess
    • Bronchiectasis
    • Tuberculois with secondary infection
    • Diffuse fibrosing alveolitis

    Cardiac

    • Infective endocarditis
    • Cyanotic heart disease
    • Congenital heart disease

    Alimentary

    • Ulcerative colitis
    • Crohn’s disease
    • Cholangiolitic cirrhosis

    Endocrine

    • Iatrogenic myxedema
    • Exophthalmic ophthalmoplegia
    • Acromegaly

    Miscellaneous

    • Hereditary
    • Idiopathic
    • Unilateral: Pancoast tumor, subclavian and innominate artery aneurysm
    • Unidigital- traumatic or tophi deposit in gout
    • Only in the upper limbs in heroin addicts due to chronic obstructive phlebitis

    Grades of Clubbing

    Grade I: Softening of nail bed
    Grade II: Obliteration of the angle of the nail bed
    Grade III: Swelling of the subcutaneous tissues over the base of the nail causing the overlying skin to become tense, shiny and wet and increasing the curvature of the nail, resulting in parrot beak or drumstick appearance.
    Grade IV: Swelling of the fingers in all dimensions associated with hypertrophic pulmonary osteoarthropathy causing pain and swelling of the hand, wrist etc, and radiographic evidence of subperiosteal new bone formation.

    Mechanism

    The exact mechanism is not known. It is believed that the stimulus for clubbing is hypoxia. Hypoxia leads to opening up of deep arteriovenous fistulas which increase the blood supply of the fingers and toes causing it to hypertrophy.

    Another hypothesis is that when reduced ferritin in venous blood escapes oxidation in the lungs and enters the systemic circulation., it causes dilation of arterio-venous anastomosis and hypertrophy of the terminal phalanx resulting in clubbing.

    Pseudoclubbing

    In hyperparathyroidism excessive bone resorption may result in disappearance of the terminal phalanges with telescoping of soft tissues and a drumstick appearance of the finger resembling clubbing. However, the curvature of the nail is not present.

    Schamroth’s test or Schamroth’s window test

    This test was originally demonstrated by South African cardiologist Dr Leo Schamroth on himself and  is a popular test for clubbing.

    When the distal phalanges (bones nearest the fingertips) of corresponding fingers of opposite hands are directly apposed (placed against each other back to back), a small diamond-shaped “window” is normally apparent between the nailbeds.

    If this window is obliterated, the test is positive and clubbing is present.