D-dimer tests

D-dimer testing is of clinical use when there is a suspicion of deep venous thrombosis (DVT) or pulmonary embolism (PE).
While a negative result practically rules out thrombosis, a positive result can indicate thrombosis but does not rule out other potential causes. Its main use, therefore, is to exclude thromboembolic disease where the probability is low. – some hospitals wont even carry out the test unless the probability is either low or moderate of thromboembolic disease.
Fibrin degradation products (FDPs) are formed whenever fibrin is broken down by enzymes (e.g., plasmin). Determining FDPs is not considered useful, as this does not indicate whether the fibrin is part of a blood clot (or being generated as part of inflammation).
D-dimers are unique in that they are the breakdown products of a fibrin mesh that has been stabilized by Factor XIII. This factor crosslinks the E-element to two D-elements. This is the final step in the generation of a thrombus.
Plasmin is a fibrinolytic enzyme that organizes clots and breaks down the fibrin mesh. It cannot, however, break down the bonds between one E and two D units. The protein fragment thus left over is a D-dimer.

D-dimer assays rely on monoclonal antibodies to bind to this specific protein fragment. Various kits have 93-95% sensitivity and about 50% specificity in the diagnosis of thrombotic disease.
• False positive readings can be due to various causes: liver disease, high rheumatoid factor, inflammation, malignancy, trauma, pregnancy, recent surgery as well as advanced age
• False negative readings can occur if the sample is taken either too early after thrombus formation or if testing is delayed for several days. Additionally, the presence of anti-coagulation can render the test negative because it prevents thrombus extension.

Chest X-rays and Pulmonary Embolism

General Rules

1. Check patient name, position, technical quality.
2. Soft tissue including breast, chest wall, companion shadow.
3. Review soft tissues and skeletal structures of shoulder girdles and chest wall.
4. Review abdomen for bowel gas, organ size, abnormal calcifications, free air, etc.
5. Review soft tissues and spine of neck.
6. Review spine and rib cage: check alignment, disc space narrowing, lytic or blastic regions, etc.
7. Review mediastinum:
A. overall size and shape
B. trachea: position
C. margins: SVC, ascending aorta, right atrium, left subclavian artery, aortic arch, main pulmonary artery, left ventricle
D. lines and stripes: paratracheal, paraspinal, paraesophageal (azygoesophageal), paraaortic
E. retrosternal clear space
8. Review hila:
A. normal relationships
B. size
9. Review lungs and pleura:
A. compare lung sizes
B. evaluate pulmonary vascular pattern: compare upper to lower lobe, right to left, normal tapering to periphery
C. pulmonary parenchyma
D. pleural surfaces
a. fissures - major and minor - if seen
b. compare hemidiaphragms
c. follow pleura around rib cage


Pulmonary Embolism
• can be done in conjunction with a ventilation-perfusion (V/Q) scan  it is difficult to diagnose pulmonary embolism on the x-ray alone
• VQ scan basically shows the parts of the lungs which are not receiving the air they should be  shows lowered perfusion

What to look out for:
• Small/medium pulmonary embolism
o Is often normal
o Linear atelectasis (partial lung collapse due to blockage)
o Blunting of the costophrenic angle (due to small effusiuon)
o Raised hemidiaphragm – present in some patients
o Wedge-shaped pulmonary infarct, abrupt cut-off of pulmonary artery, translucency of underperfused distal lung zone  rarer
o Previous infarcts – opaque linear scars
• Massive pulmonary embolism
o Pulmonary oligaemia  decrease in the size and number of pulmonary vessels due to vessel blockage or destruction
o Dilation of the pulmonary artery at the hila

- Rushmi
P.s. I have pictures, but it takes to long to stick them all up so, um, if anyone brings a laptop, can i use it? Just let me know before Friday. Thanks!

IV Fluid Chart

www.rch.org.au/emplibrary/clinicalguide/IVFLUIDCHART.pdf

Syndrome of Inappropriate Antidiuretic Hormone (SIADH)

Definition

Inappropriate secretion of ADH leading to water retention and hyponatraemia (normal 135 mmol/L)

Presentation

Plasma sodium <>

Plasma sodium <>

No oedema

Aetiology

Tumours – small cell lung carcinoma, prostate, thymus, pancreas, lymphomas

Pulmonary lesions – pneumonia, tuberculosis, lung abscess

CNS causes – meningitis, tumours, head injury, subdural haematoma, cerebral haematoma, SLE vasculitis

Metabolic causes – alcohol withdrawal, porphyria

Drugs – chlorpropamide, carbamazepine, cyclophosphamide, vincristine, phenothiazines

Diagnosis

Dilutional hyponatraemia due to excessive water retention

Low plasma osmolality with urine osmolality higher than that of plasma

Continued urinary sodium eexcretion > 30 mmol/L

No hypokalaemia (or hypotension)

Normal renal, adrenal and thyroid function

Treatment

Treat underlying cause where possible

Symptomatic relief:

1. Restrict fluid intake to 500-1000ml daily

2. Frequent measurement of plasma sodium and osmolality and bodyweight

3. If water restriction poorly tolerated or ineffective, demeclocycline may be given to inhibit action of ADH on kidney causing reversible nephrogenic diabetes insipidus

4. When syndrome very severe, rarely hypertonic saline (300 mmol/L slow i.v.) is given with furosemide – dangerous and used with extreme caution

Source: Kumar and Clark

Osmolarity vs Osmolality

Osmolality – measurement of number of osmoles of solute dissolved in each kilogram of water for a particular solution. A solution with 1 osmole of solute dissolved in 1kg of water has an osmolality of 1 osmole/kg (of water).

Osmolarity – measurement of number of osmoles of solute dissolved in each litre of a particular solution. A solution with 1 osmole of solute dissolved in water to make 1 litre of solution has an osmolarity of 1 osmole/L (of solution).

To determine osmotic pressure, osmolality is supposed to be used but for dilute solutions (e.g. body fluids) osmolarity can be used instead, as the difference is less than 1% and osmolarity is more readily measured.

Source: Guyton & Hall, Medical Physiology 11 ed.

prognosis of hyponatremia

Prognosis of hyponatremia:

Hyponatremia is a manifestation of a variety of disorders. While hyponatremia can easily be corrected, the prognosis for the underlying condition that causes it varies.

The outcome depends on the condition that is causing the problem. In general, acute hyponatremia, which occurs in less than 48 hours, is more dangerous. When sodium levels fall slowly over a period of days or weeks (chronic hyponatremia), the brain cells have time to adjust and swelling is minimal.

However, a study showed that hyponatremic patients were more than seven times as likely to die in the hospital than the control patients, and they were more than twice as likely to die after discharge. Hyponatremia appears to be an indicator of increased risk of death regardless of the disease with which it is associated.

In another study, it was found that patients who were admitted with low sodium concentration upon admission have lower mortality compared to patients admitted with normal concentration and subsequently dropped to become hyponatremic. Among the most common single cause of hyponatremia is thiazide diuretics. Other common causes of hyponatremia were loop diuretics, congestive cardiac failure and liver disease.

Investigations

FBE
- Osmolality
Decreases in hyponatraemia due to 1) sodium loss; 2) increased fluid in the bloodstream
- Sodium< 135 mmol/L

Urine test
- Osmolality
12 -14 hr fluid restriction: >850 mOsm/kg;
Affected by increased or decreased urine output
- Sodium 
May mirror serum sodium level or be the opposite depends on cause

Test result may be affected by food intake, medication e.g. diuretics, steroids, dehydration or overhydration.

Abnormal test results need further investigations to indentify cause of hyponatraemia:
If suspecting sodium loss with normal extracellular volume,
- SIADH
- Normal plasma osmolality in hyperlipidaemia / hyperproteinaemia (pseudohyponatraemia)

If suspecting an increased extracellular volume,
- Decreased urinary sodium in heart failure
- Decreased urinary sodium in liver failure
- Reduced GFR in renal diseases
- Hypoalbuminaemia?

Incidence

United States
Hyponatremia is the most common electrolyte disorder, with a marked increase among hospitalized and nursing home patients. A 1985 prospective study of inpatients in a US acute care hospital found an overall incidence of approximately 1% and a prevalence of approximately 2.5%. On the surgical ward, approximately 4.4% of postoperative patients developed hyponatremia within 1 week of surgery. Hyponatremia has also been observed in approximately 30% of patients treated in the intensive care unit.

International
Though clearly not indicative of the overall prevalence internationally, hyponatremia has been observed in as high as 42.6% of patients in a large acute care hospital in Singapore and in 30% of patients hospitalized in an acute care setting in Rotterdam.

-Hyponatremia is the most common electrolyte disorder in clinical practice. It is estimated that the incidence of hyponatremia in hospitalized patients in the U.S. is greater than one million. Hyponatremia is recognized as an independent contributor to negative patient outcomes in many chronic diseases, most notably CHF, as well as cirrhosis and SIADH.

References

http://emedicine.medscape.com/article/767624-overview
http://www.healthscout.com/ency/1/000394.html
http://au.biz.yahoo.com/070702/43/1arei.html

Electrolyte composition of intracellular and extracellular fluids, and why urine as well as serum testing is performed in a hospital setting

Firstly: the usual electrolyte levels of the ICF (intracellular fluid, the actual fluid within the cells), ISF (interstitual fluid, the fluid that bathes the cells) and Plasma (the fluid within the blood vessels) are as follows:
Plasma ISF ICF

Na+ 142 144 10
K+ 4 4 160
Ca2+ 2.5 2.5 1.5
Mg2+ 1.0 0.5 13
Cl- 102 114 2
HCO3- 26 30 8
PO42- 1.0 1.0 57
SO42- 0.5 0.5 10
Organic acid 3 4 3
Protein 16 0 55

In a 70kg male, the ICF is approximately 28L, or 35% of lean bodyweight
the ISF compirises of 12%of body weight, or 9.4L
the plasma is approximately 4.6L or 5% of total body weight.

The reason electrolyte testing of urine in addition to serum occurs in a hospital setting is to ascertain the endocrine and renal responses to the osmolar state of the patient ie. to see if the reason their sodium serum levels are low is because of renal failure, or because of excessive infusion of dextrose solution.

Complications

Complications of hyponatremia relate very closely to the symptoms of the condition itself. In reality, hyponatremia is more likely to be the complication of another condition (vomiting etc) than having complications of its own. Specifically, some complications of hyponatremia involve possibilities of coma or brain herniation, a result of the cerebral oedema, with the potential for death.

Mayoclinic
Medline

Definition of Hyponatraemia and Correction of Electrolyte Imbalances

DEFINITION OF HYPONATRAEMIA
• An abnormally low plasma sodium concentration.
• Normal = 135-145 mmol/L
• Hyponatraemia = < 135 mmol/L
• Depends on assessment of extracellular volume

CORRECTING ELECTROLYTE IMBALANCES
• Just as a note, everything I read seemed to be related to nurse care. This table seemed to sum up everything nicely, so I used it.

whats my task this week

i wasnt here yesterday, did anyone get the job of informing me of my task?

nathan

ndeng1@student.monash.edu

Management of hyponatraemia

Depends on
1 rate of development
2 severity
3 underlying cause

In RAPID development (over hours to days)
There is high morbidity due to cerebral oedema…
SO we should correct the plasma Na rapidly!
Eg. Infusion of hypertonic (3%) NaCl solutions, espescially when patient is obtunded/convulsing

HOWEVER, rapid correction in SLOW development (weeks to months) can be hazardous to the brain (cerebral cells adapted to hypo-osmolality by reducing intracellular osmolality to maintain cell vol). sudden extracellular osmolality can lead to water shifting out of cerebral neurons, abruptly reducing their volume & risking detachment from their myelin sheath. Resulting ‘myelinolysis’ can produce permanent structural/functional damage – fatal!

In SLOW development
Rate of correction should be < 10mmol/day

For underlying cause
Control source of Na loss
Eg. IV saline if warranted
Dilutional hyponatraemia – fluid restriction 600-1000ml/day
Plus withdrawal of precipitating stimulus (eg. a drug causing SIADH)

Where inadequate rise in plasma Na results, treat with demeclocycline 600-900mg/day – enhance water excretion by interfering with collecting duct responsiveness to ADH

Persistent hyponatraemia due to prolonged SIADH – oral urea therapy 30-45g/day – provides solute load to promote water excretion.

Hypovolaemic patients – diuretics with strict fluid restriction (catiously!)

With significant hyperaldosteronism – K+ sparing diuretics

Aetiology

CAUSES
An abnormally low plasma sodium level is best considered in conjunction with the person's plasma osmolarity and extracellular fluid volume status.
It is worth considering separately, the hyponatremia that occurs in the setting of diuretic use. Patients taking diuretic medications such as furosemide , hydrochlorothiazide, chlorthalidone, etc., become volume depleted. That is to say that their diuretic medicine, by design, has caused their kidneys to produce more urine than they would otherwise make. This extra urine represents blood volume that is no longer there, that has been lost from the body. As a result, their blood volume is reduced. As mentioned above, lack of adequate blood volume is a potent stimulus for ADH secretion and thence water retention.


Reduced blood volume
In patients who are volume depleted, i.e., their blood volume is too low, ADH secretion is increased, since volume depletion is a potent stimulus for ADH secretion. As a result, the kidneys of such patients recover water and produce a fairly concentrated urine. Treatment is simple (if not without risk) — simply restore the patient's blood volume, thereby turning off the stimulus for ongoing ADH release and water retention.

Exercise-associated hyponatremia
Exercise associated hyponatremia (EAH) is predominantly the occurrence of dilutional hyponatremia during or up to 24 hours after prolonged physical activity, caused by an increase in total body water relative to the amount of total body exchangeable sodium. This means consumption of fluids in excess of total body fluid losses and/or impaired renal water clearance: maximal urinary excretory rate is about 1 L/h in normal adults under resting conditions.
Inappropriate secretion of the hormone ADH, is also a contributory factor to the development of EAH. This excess hormone secretion prevents the kidneys from excreting the excess water in the urine. The primary means of avoiding EAH is to avoid excess fluid retention (weight gain during or after exercise). This can be accomplished by drinking only according to thirst and monitoring body weight before and during exercise - it is best to lose around two percent of body weight and never gain weight during exercise.
Normal blood volume
Some patients with hyponatremia have normal blood volume. In those patients, the increased ADH activity and subsequent water retention may be due to "physiologic" causes of ADH release such as pain or nausea. Alternatively, they may have the Syndrome of Inappropriate ADH. SIADH represents the sustained, non-physiologic release of ADH and most often occurs as a side effect of certain medicines, lung problems such as pneumonia or abscess, brain disease, or certain cancers (most often small cell lung carcinoma).

Increased blood volume
A third group of patients with hyponatremia are often said to be "hypervolemic". They are identified by the presence of peripheral edema. In fact, the term "hypervolemic" is misleading since their blood volume is actually low. The edema underscores the fact that fluid has left the circulation, i.e., the edema represents fluid that has exited the circulation and settled in dependent areas. Since such patients do, in fact, have reduced blood volume, and since reduced blood volume is a potent stimulus for ADH release, it is easy to see why they have retained water and become hyponatremic. Treatment of these patients involves treating the underlying disease that caused the fluid to leak out of the circulation in the first place. In many cases, this is easier said than done when one recognizes that the responsible underlying conditions are diseases such as liver cirrhosis or heart failure — conditions that are notoriously difficult to manage, let alone cure.
Recent deaths from hyponatremia have been attributed to overintake of water while under the influence of MDMA. This may also be related to inappropriate release of ADH that is stimulated by the drug.

Hypoosmolar hyponatremia
When the plasma osmolarity is low, the extracellular fluid volume status may be in one of three states: low volume, normal volume, or high volume.
Most cases of hyponatremia are associated with reduced plasma osmolarity. In fact, the vast majority of adult cases are due to increased vasopressin, i.e., anti-diuretic hormone (ADH). Vasopressin is a hormone that causes retention of water; salt is also retained but to a lesser extent. Hence, the patient with hyponatremia can be viewed as the patient with increased ADH activity. It is the physician's task to identify the cause of the increased ADH activity in each case.

Complications of chronic renal failure

1. Anaemia:

a. Erythropoietin deficiency

b. Bone marrow toxins retained in renal failure

c. Increased red cell destruction

d. Abnormal red cell membranes causing increased osmotic fragility

e. Increased blood loss due to occult gastrointestinal bleeding, blood sampling, blood loss during haemodialysis or because of platelet dysfunction

f. ACE inhibitors interfere with control of endogenous erythropoietin release.

2. Bone disease: renal osteodystrophy (various bone disease in chronic renal failure). Decreased renal production of 1a-hydoxylase enzyme leads to decreased 1,25-(OH)2D3. This results in gut calcium malabsorption.

a. Hyperparathyroid bone disease: Phosphate retention due to reduced excretion by kidney results in increased PTH synthesis and release. PTH promotes reabsorption of Ca from bone and increase renal tubular reabsorption of Ca.

b. Osteomalacia: 1,25-(OH)2D3 deficiency and hypocalcaemia impairs osteoid mineralization and cause osteomalacia.

c. Osteosclerosis: Sustained excess PTH cause increased bone density and leads to osteosclerosis.

3. Skin disease such as pruritus (itching) mainly due to retention of nitrogenous waste products of protein catabolism.

4. Gastrointestinal complications:

a. Increased risk of peptic ulceration and acute pancreatitis.

b. Constipation

Probably attributable to serum amylase elevation of up to 3 times normal due to retention of high-molecular-weight forms of amylase normally excreted in urine.

5. Metabolic abnormalities:

a. Gout: urea retention due to chronic renal failure may results in gout.

6. Cardiovascular disease

7. Cardiac failure