Monitoring of patients on TPN

Monitoring Suggested Initial Frequency2

Clinical Monitoring

Patient examination temp,pulse,RR daily

Bloop Pressure 4 hourly

Ward urine analysis daily

Fluid balance daily

Nutrient intake daily

Body weight weekly

 Laboratory monitoring

Full Blood Count daily

Prothrombin time 2 x weekly

as clinically indicated
Folate and B

Iron, transferrin, ferritin as clinically indicated

Blood urea and electrolytes, creatinine daily

Glucose daily or as indicated

Calcium, phosphate 3 x weekly

Liver function tests 2 x weekly

Magnesium, zinc, copper weekly

Acid Base measurement as clinically indicated

Urine-urea & electrolytes, creatinine (24 hour collection) as indicated

Other fluids-electrolytes (timed collection) as indicated

Bacteriology-parenteral catheter, skin puncture site as indicated

Blood Culture as indicated

Catheter tip culture on removal

Nutritional requirements for average 70 kg adult

Protein/Albumin - 4kcal/g/day
Fat - 9kcal/g/day

Note- TPN bags supplied in this hospital does not contain vitamins. Vitamin preparations e.g. Cernevit
must be prescribed separately and administered daily through a central or peripheral line. The
recommended method of infusion is in 100mls of normal saline over one hour.

The specific type of nutrition (TPN or jejunal feed etc) is not often available in short notice. Doctor in
charge must be responsible for nutrition of their patient with the help of the dietician, they must ensure
that nutrition is commenced at weekends when dietician is not available.
Reasons for the use of central lines include:

Long-term intravenous antibiotics

Long-term parenteral nutrition, especially in chronically ill persons
Long-term pain medications
Chemotherapy
Drugs that are prone to cause phlebitis in peripheral veins (caustic), such as:
Calcium chloride
Chemotherapy
Hypertonic saline
Potassium chloride (KCl)
Amiodarone
Vasopressors (for example, epinephrine, dopamine)
Plasmapheresis
Peripheral blood stem cell collections
Dialysis
Frequent blood draws
Frequent or persistent requirement for intravenous access
Need for intravenous therapy when peripheral venous accessis impossible
 Blood
Medication
Rehydration
Monitoring of the central venous pressure (CVP) in acutely ill people to quantify fluid balance[1]

2Complications

2.1Pneumothorax
2.2Bloodstream infections
2.3Thrombosis
2.4Misplacement
2.5

Rarely, small amounts of air are sucked into the vein as a result of the negative Intra-thoracic pressure and
insertion technique. Valved insertion devices can reduce this risk.[citation needed] An air embolism is the result of air
bubbles obstructing a blood vessel. Air embolisms are a very infrequent complication related to central venous
catheter removal. The threat of air embolism is minimized by proper CVC removal
with Trendelenburg positioning.[19]
Hemorrhage (profuse bleeding) and formation of a hematoma (bruise) is slightly more common in jugular venous
lines than in others.[7]
Uncommonly, the vein can fuse with the artery after being damaged by insertion of the catheter. Ultrasound use
is efficient at preventing this complication.[1]

Reversal of Anticoagulation
Anticoagulation-related major bleeding is associated with an increased risk of death and
thrombotic events, independent of the class of anticoagulant used. Although older agents of
anticoagulation and their reversal are well studied, the newer agents lack similar antidotes.
With the increasing use of nonvitamin K antagonist oral anticoagulants (NOAC), the number
of patients who require reversal of their anticoagulant effects can be expected to rise. The
following section describes the reversal agents for both older and new anticoagulants.
Heparin
Heparin has a relatively short half-life of about 6090 minutes and, therefore, the
anticoagulant effect of therapeutic doses of heparin will mostly be eliminated at 3-4 hours
after termination of continuous intravenous administration.
For a more immediate neutralization of heparin, protamine sulfate can be administered at a
dose of 1 mg for every 100 units of heparin. Protamine was originally isolated from fish sperm
and binds to heparin to form a stable, biologically inactive complex. [132, 133]
Lower molecular weight heparins
Currently, there are no specific antidotes to low molecular weight heparins. Recombinant
FVIIa (rVIIA) has been shown to stop bleeding in patients anticoagulated with fondaparinux;
however, no randomized controlled trials on such patients have been conducted.
Warfarin
Vitamin K
In patients with clinically significant bleeding, vitamin K can be used to reverse the
anticoagulant effect of vitamin K antagonists (VKA). Vitamin K can be given orally or
intravenously. The parenteral route has a more rapid onset; however, it is associated with a
slightly increased risk of allergic reaction.
Fresh frozen plasma (FFP)
In case of a life-threatening emergency, FFP can be used for the reversal of VKA. FFP
contains all the coagulation factors in normal concentrations. However, FFP should be used
with caution, as it has the potential to cause volume overload, allergic reaction, and
transfusion-related reactions (eg, transfusion-related acute lung injury). [134]
Prothrombin complex concentrates (PCCs)
In the case of serious and life-threatening bleeding, immediate correction of the international
normalized ratio (INR) can be achieved by the administration of PCCs. These contain 3 or 4
of the vitamin Kdependent coagulation factors, as well as proteins C and S. In a prospective
study, administration of PCCs has been shown to result in sustained hemostasis in patients
using VKA.
Nonvitamin K antagonist oral anticoagulants (NOACs)
The new oral anticoagulant factor Xa or IIa inhibitors have numerous advantages over
traditional vitamin K antagonists, including rapid therapeutic effectiveness, ease of dosing,
and lack of monitoring. Until recently, there were no approved drug-specific reversal agents
for the NOACs. A number of drugs are currently under development. [135, 136]
Due to the short half-life of FXa inhibitors, discontinuation of the drugs suffice in clinical
situations in which there is time to await spontaneous clearance.
Currently, PCCs can be used to address severe bleeding in patients taking NOACs when
administered in high enough dosages. Some guidelines suggest an initial dose of 25 to 50
U/kg of PCCs in life-threatening emergencies, to be repeated if necessary.
Idarucizumab (Pradbind)
Idarucizumab is a humanized antibody fragment directed against dabigatran. This agent has
been shown to completely reverse the anticoagulant effect of dabigatran within minutes; on
October 16, 2015, it was approved by the FDA as an antidote for dabigatran. [137, 138, 139, 140]
Andexanet alfa
Andexanet alfa is a recombinant, modified FXa molecule that acts as a decoy protein that is
catalytically inactive but has a high affinity for FXa inhibitors. It is being developed as an
antidote for apixaban, edoxaban, and ribaroxaban. Andexanet alfa has been shown to
reverse the anticoagulant effects of apixaban and rivroxaban in human volunteers, and more
studies are ongoing. [141]
Aripazine (PER977, ciraparantag)
Aripazine is a synthetic small molecule that has broad activity against both old (heparin, low
molecular weight heparin) and new oral anticoagulants (dabigatran, rivaroxaban, apixaban,
edoxaban). A 2014 study of human volunteers demonstrated that administration of aripazine
reversed the prolonged clotting time caused by edoxaban. Further human trials are
ongoing. [142]

The more common causes include:-

- anoxia - inhaled vomit - bronchopneumonia - peripheral circulatory failure - haemorrhage - oligaemia (pancreatitis,
mesenteric infarction) - central circulatory failure - myocardial infarction - pulmonary embolus - toxaemia - septicaemia -
drug overdose eg digoxin, opiates - cerebral causes - epilepsy - stroke

Assess patient:

circulation - peripheral circulation (cold - vasoconstriction or warm - vasodilation), blood pressure, pulse, JVP, heart
sounds,
respiration - rate, type (Cheyne-Stokes, Kussmaul etc), chest examination, is patient well oxygenated (pink)
assessment of cerebral function

If there is circulatory collapse then blood pressure is low and tachycardia. Causes include central (cardiac) failure or peripheral
failure e.g. vasodilation, oligaemia. Central failure will cause increased JVP, pulmonary oedema etc. Peripheral failure may be t
result of reduced blood volume or toxic vasodilatation.

First line investigations include:

ECG
CXR
Hb and white cell count (blood culture)
electrolytes
x-match blood if required