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.

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.

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.

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

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.

Causes of Lymphadenopathy or Enlarged Lymph Nodes

Common causes of lymphadenopathy are

I. Inflammatory Causes
A. Acute Lymphadenitis
B. Chronic Lymphadenitis:

• Septic
• Tuberculosis
• Filariasis
• Syphilis
• Lymphogranuloma inguinale

II. Neoplastic
A. Primary: Lymphosarcoma
B. Secondary: Carcinoma, sarcoma, malignant melanoma.

III. Hematological
A. Hodgkin’s disease
B. Non-Hodgkin’s lymphoma
C. Chronic lymphatic leukemia
D. AIDS

IV. Immunological

• Serum sickness
• Drug reaction
• SLE
• Rheumatoid arthritis

Differential Diagnosis

Acute Lympadenitis:

• Enlarged, tender and fixed lymph nodes.
• Overlying skin may become red, hot and brawny.
• Primary infective focus may be found.

Chronic Septic Lymphadenitis:

• Enlarged, slightly tender lymph nodes which may or may not be matted.
• If abscess has occurred, fluctuation in the centre and pitting on pressure at the periphery will be evident. It is often difficult to differentiate from tuberculous lymphadenitis.

Tuberculous Lymphadenitis:

• Commonly affects the deep cervical, mesenteric and axillary agents.
• The lymph nodes may be discrete (when it resembles chronic septic lymphadenitis) or may be matted.
  If caseation has occurred, cold abscess results which may burst forming tuberculous ulcer or sinus which takes a long time to heal.
• Fever with chills weight loss, anorexia and respiratory complaints may be present.

Syphilitic Lymphadenitis:

• Painless, firm, discrete and shotty glands which do not suppurate.
• In secondary syphilis, generalized lymphadenopathy occurs involving especially epitrochlear and occipital glands.
• Other evidence of syphilis with positive tests for syphilis like WR, VDRL, TPI, and FTA ABS.

Filarial Lymphadenitis:

• Pain, tenderness and swelling of the inguinal lymph nodes, spermatic cord and scrotum.
• Lymphangiectasia (dilation of the lymph vessels) of the inguinal region and spermatic cord.
• Eosinophilia and microfilaria can be demonstrated in the blood.
• Lymph nodes biopsy may reveal adult worm.

Lymphogranuloma Inguinale:

• Suppurative lymphadenitis with ulceration, sinus formation and extensive scarring of the inguinal lymph nodes.
• Frei’s test is confirmatory.

Lymphosarcoma:

1. Commonly affects the cervical glands which are enlarged, firm and fixed.
2. The overlying skin is stretched and shiny with dilated blue veins under it.
3. Highly malignant tumor grows rapidly and invades the surrounding tissues.

Secondary Carcinoma:

• The nodes are enlarged, irregular and fixed to all structures including the skin.
• Hard consistency.
• Primary growth may be detected.
• Patient may be cachectic and wasted.

Hodgkin’s Disease:

• Affects young adolescent males.
• Cervical glands are affected early but later all lymph nodes are involved.
• Lymph nodes are elastic and rubbery, discrete and movable with little tendency towards matting, softening or suppuration.
• Edema, venous engorgement and cyanosis of head and neck may occur due to pressure on the superior vena cava and the bronchus by the mediastinal glands. Root pains and paraplegia may develop due to pressure on the spinal cord.
• Hepatosplenomegaly and anemia occurs.
• Weight loss more than 10% of body weight and night sweats.
• Peripheral smear will show lymphocytosis and eosinophilia.
• Lymph node biopsy will show Reed Sternberg’s cell.

Non-Hodgkin’s Lymphoma:

Similar to Hodgkin’s lymphoma in clinical presentation except

• Enlargement of nodes in Waldeyer’s ring and supratrochlear glands
• Symptoms are less common
• Can be a manifestation of HIV infection
• Diagnosis confirmed by histological examination of the bone marrow.

Infectious Mononucleosis:

• Acute onset of fever, sore throat, headache, malaise and tiredness
• The lymph nodes are enlarged, discrete and slightly tender affecting especially the cervical and submandibular nodes.
• Non-tender splenomegaly may occur.
• Petechial rash may occur at the junction of soft and hard palate on the fourth day and may persist for 3-4 days.
• Peripheral smear shows leucocytosis (absolute lymphocyte count more than 1500/cmm) with atypical lymphocytosis.
• Paul-Bunnel test may be positive in 1:32 dilution or more usually in the first 10 days.

How To Look For Lymphadenopathy or Enlarged Lymph Nodes

Lymphadenopathy is defined as  inflammatory or non-inflammtory enlargement of lymph nodes.

Cervical Lymph Nodes

The lymph nodes of the neck should be examined by standing behind patient with the patient’s neck slightly flexed. The nodes must be examined from above downwards-submental, submandibular, tonsillar, cervical, posterior auricular and occipital groups.

In the left supra-clavicular fossa, a lymph node may be palpable (Virchow’s node) which occurs due to metastasis from stomach or testicular malignancy.

Axillary Lymph Nodes

The axillary glands should be examined by inserting the fingers in the axilla with the patient’s arm slightly abducted. The arm is then abducted and the apical, anterior, posterior, medial and lateral groups of lymph nodes are examined.

The supratrochlear lymph nodes

The supratrochlear lymph nodes are palpated on the medial aspect of the arm between the groove of biceps and brachialis muscle an inch above the arm fold.

The inguinal nodes

The inguinal nodes are examined in the supine position with the thigh extended. Both the medial and lateral groups of lymph nodes are examined.

Scalene nodes

Scalene nodes are present behind the sternomastoid muscle and may be palpable. In suspected malignancy, biopsy it taken from that area, even if the nodes are not palpable.

What To Examine?

Inspection:

Most of the superficial lymph nodes are visible when enlarged. The site of lymphadenopathy often gives the clue to its cause. Tuberculosis often affects the upper deep cervical nodes, secondary syphilis affects supratrochlear nodes, carcinoma of stomach affects the left supraclavicular nodes whereas filariasis affects the inguinal nodes.

The skin overlying the lymph nodes may show redness indicating underlying inflammation. Ulceration or sinus may be present in tuberculosis.

Palpation

Raised temperature tenderness is noted. If present, suggests acute inflammation. The surface is smooth normally but matted in tuberculosis and irregular in malignancy and inflammation.

The consistency of the nodes is noted. Normally it is firm.

It is rubbery in Hodgkin’s disease, firm and shotty in syphilis, matted in tuberculosis and hard in malignancy.

The mobility of the nodes is noted. Normally they are mobile and free from skin. In certain inflammatory conditions and malignancy they may be fixed and non-mobile.

Decubitus Posture In Aid Of Diagnosis

The posture a patient adopts when lying in bed often gives a valuable diagnostic clue.

Hemiplegia

A patient with hemiplegia lies in bed with one side immobile, the affected arm flexed and the affected leg extremely rotated and extended.

Meningitis and tetanus

The patient has neck stiffness and opisthotonus, a state of a severe hyperextension and spasticity.

Colic

In renal, biliary or intestinal colic, the patient is markedly restless and tossing and turning in bed in agony.

Acute inflammatory abdominal disease

The patient lies on his back quietly with legs drawn up.

Cardiorespiratory embarrassment

The patient is more comfortable in sitting-up position. This position is also assumed in abdominal destention and ascites when intra-abdominal pressure is raised.

Pneumonia and pleurisy

The patient is most comfortable lying on the affected side because the movement on the affected side is restricted.

Normal Stature and Causes of Excessive Variations

Built is the skeletal structure in relation to age and sex of the individual as compared to a normal person.

Tall Stature

A person considered to be tall when the height is greater than 2 standard deviation above the mean for the age. Gigantism is the term applied when the patient’s height is greatly in excess of the normal for his age.

There is no fixed height to constitute a giant, but in adults, it is applied for individuals with a height of more than 6 ½ ft.

Causes of Gigantism

1. Simple or primary gigantism: Racial, familial or constitutional.
2. Endocrine: Hyperpituitarism, hypogonadis,.
3. Genetic: Klinefelter’s syndrome.
4. Metabolic: Marfan’s syndrome, homocystinuria.
5. Miscellaneous: Cerebral gigantism, overeating.

Constitutional

Usually in constitutional tall stature the parents are also tall. q

Hyperpituitarism

In thisthe patient is very tall but with normal body properties. However, the features are coarse with increased heel pad thickness. There may be evidence of raised intracranial tension.

Cerebral Gigantism

Children with cerebral gigantism (Soto’s syndrome) have a large elongated head, prominent forehead, large ears and jaws, elongated chin, antimongoloid slant to the eyes and coarse facial features. They have subnormal intelligence and impaired coordination. The cause of this disorder is not known.

Sexual Precocity and Virilizing Disorders

In these children, acceleration of linear growth occurs simultaneously with signs of premature sexual development or inappropriate virilization. This disorder may be due to congenital adrenal hyperplasia, adrenal tumor, gonadal tumor or premature secretion of gonadotropic hormones. The bone age is usually advanced so that the adult stature may be diminished.

Marfan’s syndrome

These patients are tall with long limbs, narrow hands, long slender fingers (arachnodactyly), hyperextensible joints, dislocation of the lens, high arched plate, kyphoscoliois, arm span greater than the height and the lower segment more than the upper segment.

Homocystinuria

This condition resembles Marfan’s syndrome.

Klinefelter’s Syndrome

1. Lower segment more than the upper segment.
2. Gynecomastia
3. Small, firm testes, azoospermia.
4. Chromation (Barr) body usually present. (Some may be chromatin negative).
5. Mental retardation
6. Associated with Mongolism and Leukemia.
7. Chronic pulmonary disease, varicose veins and diabetes are more common.

Dwarfism

Dwarfism is the term applied when the patient’s height is far less than normal for his age and sex. It is usually applied for adults below 4 ½ ft. in height.

Causes

1. Hereditary
2. Chromosomal: Turner’s syndrome, Down’s syndrome, etc.
3. Constitutional delayed growth and puberty.
4. Nutritional: Malnutrition, malabsorption, rickets
5. Endocrine: Hypopituitarism, hypothyroidism, excessive androgens and glucocorticoidism, congenital adrenal hyperplasia, insulin deficiency
6. Skeletal: Achondroplasia, spinal deformities
7. Systemic diseases: Renal tubular acidosis, uremia, congenital cyanotic heart disease, cirrhosis of liver, etc.

Hereditary

In hereditary short stature there is no endocrine abnormality. The bone age and the dental age are normal. Although they are short, they grow at a constant rare of 4-5 cms, a year and they have normal body proportions for age. This may be either genetic (if there is a family history of short stature), or primordial (if there is no family history of short stature).

Constitutional delayed growth and puberty

This disorder is common among adolescent boys. There is no true endocrine deficiency. They grow at a constant rate of about 4 cm a year but their bone age and dental age are delayed by about 2 years. Often there is a history of delay in growth and pubertal development in the father and other male relatives.

Turner’s syndrome

These children are predominantly girls. They have agenesis of their gonads. The chromosomal pattern is 45+XO. They have a characteristically short webbed neck, low hair line, square and shield-like chest, cubitus valgus and mental retardation. Although short, they grow at the rate of 4 cm each year with normal bone age and dental age but absent pubertal growth spurt, so that during adolescence, the skeletal age is delayed due to the absence of sex hormones (streak ovaries).

Hypopituitarism

These children have the skeletal age and the dental age delayed by more than 2 years. The growth rate is less than 4 cm/year. The ratio of the upper segment and the lower segment is normal.

Hypothyroidism

These children have mental, dental and skeletal retardation since birth. There would be course dry skin and constipation. Their body proportion is infantile i.e., upper segment is more than lower segment.

Achondroplasia

Achondroplasia dwarfs have short limbs resulting in short stature. Hence, the lower segment is always less than the upper segment. Their mental and dental ages are normal and so are the endocrine functions.

Systemic disease

Most chronic systemic disease can cause growth failure during childhood. These illnesses can be recognized by their own specific clinical features and growth failure is a secondary problem.

What is Jaundice and When Does It Occur

Jaundice is a symptom complex which is characterized by yellow coloration of tissues and body fluids due to an increase in bile pigments i.e. Bilrubin and related products

It may arise due to:

• Increased bile pigment load to the liver.
• Affection of bilirubin diffusion into the liver cells.
• Defective conjugation.
• Defective excretion.

Other causes of yellow coloration of tissues

Yellow coloration of tissues can occur due to carotenemia and mepacrine therapy.

Bilirubin Metabolism

1. Breakdown phase: Hemoglobin released by breakdown of aged cells is broken down into globin and heme. The heme is further broken into iron and bilirubin. Bilirubin attaches to serum albumin and is transported to the liver where it is taken up.
2. Conjugation phase: In the liver, bilirubin is separated from albumin and conjugated to glucuronide by glucuronyl transferase. The conjugated bilirubin is water soluble and can be excreted by kidneys.
3. Alimentary phase: The conjugated bilirubin is excreted through the bile canaliculi and reaches the intestines where it is converted to stercobilinogen and urobilinogen by the intestinal bacteria. About 70% of this is absorbed in the colon and brought back to the liver and re-excreted (enterohepatic circulation). Unabsorbed stercobilinogen gives brown color to the faces.
4. Excretion phase: Circulating urobilinogen is carried to the kidneys for excretion in the urine as urobilinogen.

Normal values

Serum bilirubin: Total: 1 mg%; Direct: 0.25 mg%. Urinary bilirubin is present if direct bilirubin is greater than 0.4 mg% in serum.

Urine Urobilinogen: 100-200 mg/day.

Fecal stercobilinogen: 300 mg/day

Distribution of Jaundice

High concentration of bilirubin (hyperbilirubinemia), the bile product and its congeners are responsible for yellow discoloratrion of skin in jaundice. They bind with circulating proteins.

Bilirubin has more affinity for nervous tissue like basal ganglia and elastic tissues such as skin, sclera and blood vessels.

Infections:

• Viral hepatitis
• Weil’s disease (Leptospirosis)
• Septicemia
• Malaria
• Typhoid

Toxicity

• Anesthetic agents: Halothane, chloroform
• Anticoagulants: Phenindione
• Anti-tuberculous drugs: Rifampicin, P.A.S., I.N.H., Thiacetazone
• Metals: Arsenic, mercury, gold, bismuth
• Chemicals: DDT
• X-ray irradiations

Cirrhosis

• Portal Hypertension
• Biliary cirrhosis
• Hemochromatosis

Extra Hepatic Obstruction

• Stone
• Stricture
• Parasites
• Acute cholecystitis
• Carcinoma of the head of the pancreas
• Neoplasm of bile ducts, gall bladder and ampulla of Vater
• Congenital: Biliary atresia

Intra Hepatic Obstruction
1. Cholestatic phase of infective hepatitis
2. Drugs – Steroids, chlorpromazine, PAS, sulfonamides, chlorpropamide tolbutamide, methyl testosterone

Hemolytic Causes of Jaundice

There is an increased destruction of red blood cells which causes increase in production of bilirubin. This may occur due to

• Infections like Malaria, Clostridium welchi
• Drugs like L. Methyldopa, quinine, phenacetin, sulfonamides
• Burns
• Irradiation
• Poisons as in: Snake Venom, Favism
• Mismatched blood-tranfusion
• Paroxysmal Cold Hemoglobinuria
• Lymphoma
• Leukemia
• Systemic lupus erythematosis
• Uremia

Congenital Hyperbilirubinemia

• Gilbert’s syndrome
• Crigler-Najjar syndrome
• Dubin Johnson syndrome
• Rotor’s syndrome.

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