The full article

Can CBD help treat a fever?

Fever is a condition characterized by an increase in the temperature of the human body from the normal range, which is around 36-37 degrees centigrade. It is regarded as a typical medical sign and sometimes referred to as controlled hyperthermia or pyrexia.

The change in the body’s temperature is commonly associated with the brain’s hypothalamus. It acts as the body’s thermostat. When everything inside the body works well, it sets the temperature to normal. The hypothalamus sets the body’s temperature to higher than normal when it is not healthy and thus, a fever occurs(1).

Fever causes a person to feel physical discomfort and become weak. Other symptoms include headache, sweating, irritability, chills, and muscle aches(2)

Contrary to what most people think, a fever is not an illness. It is regarded as one of the body’s ways of fighting infection. Generally, it goes away after a few days, and the body temperature can be lowered down to normal levels by taking over-the-counter medications.

Fever is not considered a serious condition. However, a child with a fever accompanied by irritable movements and repeated vomiting should immediately see a doctor. An adult with a body temperature that reaches 39.4 should also seek medical help immediately. 

CBD for Fever: What is known so far 

Fever develops when the hypothalamus strategically increases the body’s temperature. This happens when the body is fighting infections, but can also occur in response to medications, immunizations, or diseases such as cancer. Among the most common of these are those caused by bacterias and viruses.  

Earlier animal research hinted that fever triggered by a virus could be treated using CBD(3).

Also, the use of CBD oil may be an effective option in the treatment of fever caused by a massive inflammatory reaction. The CBD oil triggers the body’s anti-inflammatory response via the endocannabinoid system(4).

Is CBD oil going to strengthen or weaken your immune system? The answer is that it can do both. 

It depends on the person’s autoimmune condition. One’s immune system may overreact to non-threatening internal or threatening external events, which may lead to an attack against the healthy cells in the body in an attempt to eradicate the threat. Choose the best natural CBD product if you’re living with an autoimmune disease(5).

Another research conducted found out that CBD has anti-inflammatory properties (6). These allow the compound to reduce pains and aches. CBD also relaxes the body and helps some people with insomnia.

Due to the abundance of potential benefits that cannabis and CBD use can provide, many studies were and are being conducted to verify these. The majority of the said studies are well funded and expected to provide significant findings soon.

Among the most significant aspects that CBD-centered studies are focusing on right now is the effect of the compound in strengthening a person’s immune system. This premise is based on the fact that a strong immune system is quite effective in combating infections that typically leads to fever. 

Conclusion

Though over-the-counter medicine does what it can to relieve fever, it may not be enough for some users. With cannabidiol (CBD) as a medication making headlines, many people wonder if it can help with common medical conditions such as fever.

Research suggests that CBD may be used to treat fever caused by pathogens.

Thus, when considering the idea of buying CBD oil, it is important for a person to take his or her health goals into account. This technique is beneficial in deciding the best type of CBD oil to have. More importantly, consult with a doctor experienced in CBD use for professional advice before deciding on any particular product.


  1. Fever, What Is It? By Harvard Health Publishing (2018, October) Retrieved from https://www.health.harvard.edu/a_to_z/fever-a-to-z
  2. Patient Care and Health Information – Fever. (2017, July 21) Retrieved from https://www.mayoclinic.org/diseases-conditions/fever/symptoms-causes/syc-20352759
  3. A Novel Role of Cannabinoids: Implication in the Fever Induced by Bacterial Lipopolysaccharide. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/17194800
  4. ibid.
  5. Nagarkatti, P., Pandey, R., Rieder, S. A., Hegde, V. L., & Nagarkatti, M. (2009). Cannabinoids as novel anti-inflammatory drugs. Future medicinal chemistry, 1(7), 1333–1349. https://doi.org/10.4155/fmc.09.93
  6. The Health Effects of Cannabis and Cannabinoids: The Current State of Evidence and Recommendations for Research. Retrieved from https://www.ncbi.nlm.nih.gov/books/NBK425755/

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Thevetia peruviana

  1. NAME

   1.1 Scientific name

   1.2 Family

   1.3 Common name(s)

  1. SUMMARY

   2.1 Main risks and target organs

   2.2 Summary of clinical effects

   2.3 Diagnosis

   2.4 First-aid measures and management principles

   2.5 Poisonous parts

   2.6 Main toxins

  1. CHARACTERISTICS

   3.1 Description of the plant

      3.1.1 Special identification features

      3.1.2 Habitat

      3.1.3 Distribution

   3.2 Poisonous parts of the plant

   3.3 The toxin(s)

      3.3.1 Name(s)

      3.3.2 Description, chemical structure, stability

      3.3.3 Other physico-chemical characteristics

   3.4 Other chemical contents of the plant

  1. USES/CIRCUMSTANCES OF POISONING

   4.1 Uses

   4.2 High risk circumstances

   4.3 High risk geographical areas

  1. ROUTES OF ENTRY

   5.1 Oral

   5.2 Inhalation

   5.3 Dermal

   5.4 Eye

   5.5 Parenteral

   5.6 Others

  1. KINETICS

   6.1 Absorption by route of exposure

   6.2 Distribution by route of exposure

   6.3 Biological half-life by route of exposure

   6.4 Metabolism

   6.5 Elimination by route of exposure

  1. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY

   7.1 Mode of action

   7.2 Toxicity

      7.2.1 Human data

         7.2.1.1 Adults

         7.2.1.2 Children

      7.2.2 Animal data

      7.2.3 Relevant in vitro data

   7.3 Carcinogenicity

   7.4 Teratogenicity

   7.5 Mutagenicity

   7.6 Interactions

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

   8.1 Material sampling plan

      8.1.1 Sampling and specimen collection

         8.1.1.1 Toxicological analyses

         8.1.1.2 Biomedical analyses

         8.1.1.3 Arterial blood gas analysis

         8.1.1.4 Haematological analyses

         8.1.1.5 Other (unspecified) analyses

      8.1.2 Storage of laboratory samples and specimens

         8.1.2.1 Toxicological analyses

         8.1.2.2 Biomedical analyses

         8.1.2.3 Arterial blood gas analysis

         8.1.2.4 Haematological analyses

         8.1.2.5 Other (unspecified) analyses

      8.1.3 Transport of laboratory samples and specimens

         8.1.3.1 Toxicological analyses

         8.1.3.2 Biomedical analyses

         8.1.3.3 Arterial blood gas analysis

         8.1.3.4 Haematological analyses

         8.1.3.5 Other (unspecified) analyses

   8.2 Toxicological Analyses and Their Interpretation

      8.2.1 Tests on toxic ingredient(s) of material

         8.2.1.1 Simple Qualitative Test(s)

         8.2.1.2 Advanced Qualitative Confirmation Test(s)

         8.2.1.3 Simple Quantitative Method(s)

         8.2.1.4 Advanced Quantitative Method(s)

      8.2.2 Tests for biological specimens

         8.2.2.1 Simple Qualitative Test(s)

         8.2.2.2 Advanced Qualitative Confirmation Test(s)

         8.2.2.3 Simple Quantitative Method(s)

         8.2.2.4 Advanced Quantitative Method(s)

         8.2.2.5 Other Dedicated Method(s)

      8.2.3 Interpretation of toxicological analyses

   8.3 Biomedical investigations and their interpretation

      8.3.1 Biochemical analysis

         8.3.1.1 Blood, plasma or serum

         8.3.1.2 Urine

         8.3.1.3 Other fluids

      8.3.2 Arterial blood gas analyses

      8.3.3 Haematological analyses

      8.3.4 Interpretation of biomedical investigations

   8.4 Other biomedical (diagnostic) investigations and their interpretation

   8.5 Overall Interpretation of all toxicological analyses and toxicological investigations

   8.6 References

  1. CLINICAL EFFECTS

   9.1 Acute poisoning

      9.1.1 Ingestion

      9.1.2 Inhalation

      9.1.3 Skin exposure

      9.1.4 Eye contact

      9.1.5 Parenteral exposure

      9.1.6 Other

   9.2 Chronic poisoning

      9.2.1 Ingestion

      9.2.2 Inhalation

      9.2.3 Skin exposure

      9.2.4 Eye contact

      9.2.5 Parenteral exposure

      9.2.6 Other

   9.3 Course, prognosis, cause of death

   9.4 Systematic description of clinical effects

      9.4.1 Cardiovascular

      9.4.2 Respiratory

      9.4.3 Neurological

         9.4.3.1 CNS

         9.4.3.2 Peripheral nervous system

         9.4.3.3 Autonomic nervous system

         9.4.3.4 Skeletal and smooth muscle

      9.4.4 Gastrointestinal

      9.4.5 Hepatic

      9.4.6 Urinary

         9.4.6.1 Renal

         9.4.6.2 Others

      9.4.7 Endocrine and reproductive systems

      9.4.8 Dermatological

      9.4.9 Eye, ears, nose, throat: local effects

      9.4.10 Haematological

      9.4.11 Immunological

      9.4.12 Metabolic

         9.4.12.1 Acid base disturbances

         9.4.12.2 Fluid and electrolyte disturbances

         9.4.12.3 Others

      9.4.13 Allergic reactions

      9.4.14 Other clinical effects

      9.4.15 Special risks

   9.5 Others

   9.6 Summary

  1. MANAGEMENT

   10.1 General principles

   10.2 Relevant laboratory analyses and other investigations

      10.2.1 Sample collection

      10.2.2 Biomedical analysis

      10.2.3 Toxicological/toxinological analysis

      10.2.4 Other investigations

   10.3 Life supportive procedures and symptomatic treatment

   10.4 Decontamination

   10.5 Elimination

   10.6 Antidote/antitoxin treatment

      10.6.1 Adults

      10.6.2 Children

   10.7 Management discussion

  1. ILLUSTRATIVE CASES

   11.1 Case reports from literature

   11.2 Internally extracted data on cases

   11.3 Internal cases

  1. ADDITIONAL INFORMATION

   12.1 Availability of antidotes/antitoxins

   12.2 Specific preventive measures

   12.3 Other

  1. REFERENCES

   13.1 Clinical and toxicological

   13.2 Botanical

  1. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE ADDRESS(ES)

 

    POISONOUS PLANTS

  1. NAME

     1.1 Scientific name

       Thevetia peruviana (pers).  K Shum

     1.2 Family

       Apocynaceae

     1.3 Common name(s)

       Be still Tree

       Digoxin

       Lucky Nut

       Nerium oleander

       Yellow Oleander

  1. SUMMARY

     2.1 Main risks and target organs

       The main toxic effects of glycosides found in Thevetia 

       peruviana are  related to its digitalis-like action on the 

       heart and severe  gastrointestinal irritation. 

     2.2 Summary of clinical effects

       The common presenting symptoms are: numbness, burning of the 

       mouth,  nausea, vomiting, abdominal pain and diarrhoea.  Other 

       features seen are:   drowsiness, coma, occasional convulsions, 

       and cardiac arrhythmias. Death is  due to ventricular 

       fibrillation.

     2.3 Diagnosis

       Diagnosis depends on the patient’s history and the clinical  

       presentation.

       

       Cardiac glycosides can be investigated in the blood by 

       competitive  immunoassay.  The serum potassium concentration 

       should be monitored.   Electrocardiography, frequent serum 

       electrolytes (especially potassium concentration), and renal 

       function tests  are essential investigations.  Remnants of 

       seeds, vomitus or gastric  aspirate should be collected for 

       identification purposes.

     2.4 First-aid measures and management principles

       Admit the patient to a hospital.  Treatment should aim at a) 

       gut  contamination by emesis or lavage if the ingestion is 

       recent; b) correction  of electrolyte imbalance; c) correction 

       of severe bradycardia with atropine  or electrical pacing and 

       correction of ventricular dysrrhythmias; and d)  

       administration of digoxin Fab antibodies if available.

     2.5 Poisonous parts

       All parts of the plant, particularly the seeds are poisonous 

       owing to  the presence of cardiac glycosides or cardiac toxins 

       which act directly on  the heart.  Ingestion of these plant 

       parts could lead to death.  The whole  plant exudes in a milky 

       juice which is very poisonous.

     2.6 Main toxins

       Thevetin A, Thevetin B and Peruvoside.

  1. CHARACTERISTICS

     3.1 Description of the plant

       3.1.1 Special identification features

             It is a small ornamental tree which grows to about 10 to 

             15  feet high.  The leaves are spirally arranged, linear 

             and about 13  to 15 cm in length.  Flowers are bright 

             yellow and funnel-shaped  with 5 petals spirally 

 

             twisted.  The fruits are somewhat globular,  slightly 

             fleshy and have a diameter of 4 to 5 cm.  The fruits,  

             which are green in colour, become black on ripening.  

             Each fruit  contains a nut which is longitudinally and 

             transversely divided.   All parts of the plant contain 

             the milky juice.

       3.1.2 Habitat

             Grown as an ornamental tree in gardens.

       3.1.3 Distribution

             This plant is native of Central & South America, but now 

             frequently grown throughout the tropical and sub-

             tropical regions.

     3.2 Poisonous parts of the plant

       All parts of the plant are poisonous, especially the kernels 

       of the  fruit. 

       

       The absorption of the equivalent of two Thevetia peruviana 

       leaves may be  sufficient to kill a 12.5 kg child (Ellenhorn 

       and Barceloux, 1988).

     3.3 The toxin(s)

       3.3.1 Name(s)

             Cardiac glycosides, Thevetin A & B, Thevetoxin, 

             Peruvoside,  Ruvoside and Nerifolin are found in  T. 

             Peruviana (Arnold et al.,  1935).

       3.3.2 Description, chemical structure, stability

             Thevetin A = C42H64O19; MW = 872.93;

             

                  CAS number: 37933-66-7

             

             Thevetin B = C42H66O18; MW = 858.95;

             

                  CAS number: 11005-70-2

             

             Peruvoside = C42H44O9; MW = 548.65; 

             

                  CAS number: 1182-87-8

             

             Peruvoside is freely soluble in methanol and ethanol and 

             sparingly  soluble in chloroform acetone (Merck Index, 

             1976).

       3.3.3 Other physico-chemical characteristics

             No data available.

     3.4 Other chemical contents of the plant

       No data available.

  1. USES/CIRCUMSTANCES OF POISONING

     4.1 Uses

       The plant is widely grown as an ornamental tree to adorn 

       gardens and at  religious sites for offerings.

       

       The cardiac glycoside peruvoside from yellow oleander is 

       used medicinally  for treatment of cardiac insufficiency,

       (Frohne & Pfander, 1983).  However,  it has been found 

       that the margin between the therapeutic and the toxic 

       dose is too small for thevetin to be therapeutically 

       useful (Watt &  Breyer-Bradwijk, 1962).

     4.2 High risk circumstances

 

       Children have easy access to this plant in gardens or  

       hedgerows, and they may play with and taste the bright yellow 

       flowers and the conspicuous green fruit.

       

       The kernel of the seeds is used in suicide attempts, 

       particularly by young people and especially in northern parts 

       of Sri Lanka.  Sometimes it is taken with alcoholic drinks 

       (Shaw and Pearn, 1979).

     4.3 High risk geographical areas

       This plant is a native of Central and South America, but is 

       now frequently grown in parks and gardens in tropical and 

       subtropical areas.

  1. ROUTES OF ENTRY

     5.1 Oral

       Accidental ingestion of the seeds by children may cause 

       poisoning.   Suicidal ingestion is also common in some areas.  

     5.2 Inhalation

       No data available.

     5.3 Dermal

       No data available.

     5.4 Eye

       No data available.

     5.5 Parenteral

       No data available.

     5.6 Others

       No data available.

  1. KINETICS

     6.1 Absorption by route of exposure

       Thevetin is easily absorbed from the gastrointestinal tract.

     6.2 Distribution by route of exposure

       Thevetin glycosides occur in higher concentrations in heart 

       muscle than  in blood (Ellenhorn and Barceloux, 1988).

     6.3 Biological half-life by route of exposure

       Thevetin probably has a shorter half-life than digoxin and a 

       lower risk  of accumulation in the body (Arnold et al., 1935).

     6.4 Metabolism

       No data available.

     6.5 Elimination by route of exposure

       No human data available.

  1. TOXICOLOGY/TOXINOLOGY/PHARMACOLOGY

     7.1 Mode of action

       Cardiac glycosides exert a digoxin-like effect by inhibiting 

       the  sodium-potassium adenosine-triphosphatase (ATP) enzyme 

       systems.  The  increased intracellular sodium concentration 

       and the increased serum potassium concentration produce 

       negative chronotropic  and positive inotropic effect (Shaw and 

       Pearn, 1979).  The resulting toxic  syndrome resembles 

       digitalis poisoning with marked hyperkalaemia, conduction 

       abnormalities and  ventricular arrhythmias (Ellenhorn and 

       Barceloux, 1988).

     7.2 Toxicity

       7.2.1 Human data

             7.2.1.1 Adults

                     The kernels of about 10 fruits may be fatal  

                     (Saravanapavananthan, 1985). 

             7.2.1.2 Children

 

                     The kernel of one fruit may be fatal  

                     (Saravanapavananthan, 1985).

       7.2.2 Animal data

             Cattle grazing on grass under Thevetia peruviana trees 

             are  known to have died (Saravanapavananthan 1985) and 

             nuts are lethal  to chickens (Arnold et al., 1935).

       7.2.3 Relevant in vitro data

             No data available.

     7.3 Carcinogenicity

       No data available.

     7.4 Teratogenicity

       No data available.

     7.5 Mutagenicity

       No data available.

     7.6 Interactions

       Pre-medication with digoxin or other cardiac glycosides 

       increases the  severity of poisoning.  The interaction between 

       digoxin and quinidine  (increasing digoxin levels) may also 

       occur with Thevetia glycosides. 

  1. TOXICOLOGICAL/TOXINOLOGICAL ANALYSES AND BIOMEDICAL INVESTIGATIONS

     8.1 Material sampling plan

       8.1.1 Sampling and specimen collection

             8.1.1.1 Toxicological analyses

             8.1.1.2 Biomedical analyses

             8.1.1.3 Arterial blood gas analysis

             8.1.1.4 Haematological analyses

             8.1.1.5 Other (unspecified) analyses

       8.1.2 Storage of laboratory samples and specimens

             8.1.2.1 Toxicological analyses

             8.1.2.2 Biomedical analyses

             8.1.2.3 Arterial blood gas analysis

             8.1.2.4 Haematological analyses

             8.1.2.5 Other (unspecified) analyses

       8.1.3 Transport of laboratory samples and specimens

             8.1.3.1 Toxicological analyses

             8.1.3.2 Biomedical analyses

             8.1.3.3 Arterial blood gas analysis

             8.1.3.4 Haematological analyses

             8.1.3.5 Other (unspecified) analyses

     8.2 Toxicological Analyses and Their Interpretation

       8.2.1 Tests on toxic ingredient(s) of material

             8.2.1.1 Simple Qualitative Test(s)

             8.2.1.2 Advanced Qualitative Confirmation Test(s)

             8.2.1.3 Simple Quantitative Method(s)

             8.2.1.4 Advanced Quantitative Method(s)

       8.2.2 Tests for biological specimens

             8.2.2.1 Simple Qualitative Test(s)

             8.2.2.2 Advanced Qualitative Confirmation Test(s)

             8.2.2.3 Simple Quantitative Method(s)

             8.2.2.4 Advanced Quantitative Method(s)

             8.2.2.5 Other Dedicated Method(s)

       8.2.3 Interpretation of toxicological analyses

     8.3 Biomedical investigations and their interpretation

       8.3.1 Biochemical analysis

             8.3.1.1 Blood, plasma or serum

             8.3.1.2 Urine

 

             8.3.1.3 Other fluids

       8.3.2 Arterial blood gas analyses

       8.3.3 Haematological analyses

       8.3.4 Interpretation of biomedical investigations

     8.4 Other biomedical (diagnostic) investigations and their 

       interpretation

     8.5 Overall Interpretation of all toxicological analyses and 

       toxicological investigations

     8.6 References

  1. CLINICAL EFFECTS

     9.1 Acute poisoning

       9.1.1 Ingestion

             Thevetia peruviana poisoning closely resembles digitalis 

              poisoning, with gastrointestinal and cardiac symptoms.

             

             Local irritation of mucous membranes and mouth is 

             followed by  nausea, vomiting and giddiness within 

             hours.  Other clinical  features are: severe diarrhoea, 

             abdominal pain, dilated pupils and  occasionally 

             convulsions.  Cardiovascular manifestations range from 

             sinus bradycardia with sino-atrial-block, first and 

             second degree heart block, junctional rhythms, A-V block,

              atrial and ventricular ectopic beats, and ventricular 

             fibrillation.

       9.1.2 Inhalation

             No data available.

       9.1.3 Skin exposure

             Burning sensation of the skin due to the sap.

       9.1.4 Eye contact

             Severe eye irritation caused by the sap is possible.

       9.1.5 Parenteral exposure

             No data available.

       9.1.6 Other

             No data available.

     9.2 Chronic poisoning

       9.2.1 Ingestion

             No data available.

       9.2.2 Inhalation

             No data available.

       9.2.3 Skin exposure

             No data available.

       9.2.4 Eye contact

             No data available.

       9.2.5 Parenteral exposure

             No data available.

       9.2.6 Other

             No data available.

     9.3 Course, prognosis, cause of death

       In severe poisoning, diarrhoea, vomiting, abdominal pain and 

       sinus  bradycardia are early features.  Hyperkalaemia, 

       conduction block and  ventricular ectopics indicate serious 

       toxicity (Ellenhorn & Barceloux,  1988).

       

       

       Indicators of a poor prognosis include multiple and varying 

       cardiac rhythms  occur, with sinoatrial and atrio-ventricular 

 

       blocks in combination with ventricular excitability, ST 

       depression over 2.5 mm and response to atropine 

       (Saravanapavananthan &  Ganeshmoorthy, 1986).

       

       Conduction block and sinus bradycardia may persist for 5 days 

       after  ingestion.  Patients usually recover from these if no 

       underlying  cardiovascular pathology exist (Ellenhorn & 

       Barceloux, 1988).

       

       The usual cause of death is ventricular fibrillation.

     9.4 Systematic description of clinical effects

       9.4.1 Cardiovascular

             The main actions of thevetin and other cardiac 

             glycosides  are on the heart.  In mammalian heart, low 

             doses of thevetin have a stimulant action, and large  

             doses depress and stop ventricular contraction (Arnold 

             et al.,  1935).

             

             ECG changes include: sinus bradycardia, inversion of T 

             waves, P-R prolongation, A-V dissociation, ventricular 

             tachycardia and ultimately ventricular fibrillation, 

             which is the usual cause of death.

       9.4.2 Respiratory

             Thevetin has little, if any, direct effect on 

             respiration  (Watt and Breyer-Branwijk, 1962).

       9.4.3 Neurological

             9.4.3.1 CNS

                     Mydriasis, drowsiness, coma, and occasionally  

                     convulsions.

             9.4.3.2 Peripheral nervous system

                     Paraesthesia and weakness have been reported 

                     even  in the early phase. (Ellenhorn & Barceloux,

                      1988).

             9.4.3.3 Autonomic nervous system

                     Pupils may be dilated (Duke, 1987) and excessive 

                      salivation has been reported (Ellenhorn & 

                     Barceloux,  1988).

             9.4.3.4 Skeletal and smooth muscle

                     Thevetin has a direct stimulant action on the  

                     smooth muscles of the intestine bladder, uterus 

                     and blood  vessel walls (Watt & Breyer-Branwijk, 

                     1962).

                     

                     

                     Skeletal muscle hypertonia has also been 

                     reported  (Ellenhorn & Barceloux).

       9.4.4 Gastrointestinal

             Nausea, intense vomiting and diarrhoea.

       9.4.5 Hepatic

             No data available.

       9.4.6 Urinary

             9.4.6.1 Renal

                     Acute renal failure may occur secondary to  

                     cardiogenic shock.

             9.4.6.2 Others

                     No data available.

 

       9.4.7 Endocrine and reproductive systems

             The seed is used as an abortifacient in Bengal and  

             neighbouring provinces (Watt & Breyer-Bradwijk, 1962).

       9.4.8 Dermatological

             Irritant to skin.

       9.4.9 Eye, ears, nose, throat:  local effects

             Burning sensation and dryness of throat could occur.

       9.4.10 Haematological

              No data available.

       9.4.11 Immunological

              No data available.

       9.4.12 Metabolic

              9.4.12.1 Acid base disturbances

                       Circulatory collapse could cause metabolic  

                       acidosis.

              9.4.12.2 Fluid and electrolyte disturbances

                       Gastrointestinal fluid loss often leads to  

                       dehydration and hypovolaemic shock.  Hyperkalaemia 

                       is seen in severe poisoning.

              9.4.12.3 Others

                       No data available.

       9.4.13 Allergic reactions

              No data available.

       9.4.14 Other clinical effects

              No data available.

       9.4.15 Special risks

              Pregnancy: No data available

              Breast feeding: No data available

              Enzyme deficiencies: No data available

     9.5 Others

       No data available.

     9.6 Summary

  1. MANAGEMENT

      10.1 General principles

         Admit the patient to a hospital immediately.  In severe 

         poisoning,  admit to an Intensive Care Unit for immediate 

         cardiac monitoring.  Treatment  usually depends on the 

         severity of poisoning and includes: immediate gastric  

         decontamination, and correction of arrhythmias and 

         electrolyte disturbance.

         

         Frequent electrocardiograms or continuous cardiac monitoring 

         are necessary.  Check electrolytes regularly, particularly 

         serum potassium levels.

      10.2 Relevant laboratory analyses and other investigations

         10.2.1 Sample collection

                Remaining parts of the ingested plant  (fruit, flower,

                 branches with leaves) and gastric contents are 

                useful for botanical  identification. Plant portions 

                found in vomitus should be stored in  a plastic bag 

                for the laboratory.

         10.2.2 Biomedical analysis

                ECG is valuable for diagnosis, prognosis and 

                treatment, and  shows changes similar to those

                produced by digitalis glycosides.  

                

 

                In moderate to severe poisoning check serum 

                electrolytes  (especially serum potassium),and

                monitor renal function. Arterial blood gases should 

                be determined.

         10.2.3 Toxicological/toxinological analysis

                Digoxin immunoassay can be used to detect Thevetin  

                poisoning.

         10.2.4 Other investigations

      10.3 Life supportive procedures and symptomatic treatment

         Prolonged repeated ECG monitoring is required in serious 

         cases.

         

         Ensure adequate airway and ventilation.

         

         Give adequate oral or IV fluids and correct any electrolyte 

         imbalance.  If  serum potassium level exceeds 6 mmol/l give 

         50 ml of 50% glucose and  initially 10 units of soluble 

         insulin IV.

         

         Treatment is determined by the presence of cardiotoxicity. 

         Bradycardia may require atropine or electrical pacing.  

         Ventricular arrhythmias may be be  controled with lidocaine 

         or, less appropriately, phenytoin.  

         

         Phenytoin should be infused slowly IV (at a rate no greater 

         than 50  mg/minute) until dysrrhythmias are controlled, to a 

         maximum total dose of  1000 mg (adult). 

         

         Lidocaine may be administered as 1 mg/kg IV bolus, followed 

         by continuous  infusion of 1 to 4 mg/minute (adult).

         

         Treatment of hyperkalemia should aim at lowering the serum 

         potassium level,  with insulin, glucose, NaHCO3 and ion-

         exchange resins.  Hemoperfusion may be considered in severe 

         cases.  Calcium chloride is contraindicated (Goldfrank,  

         1986).

      10.4 Decontamination

         If consciousness is not impaired, induce emesis or perform 

         gastric  lavage.

         

         After emesis or gastric lavage, give oral activated charcoal,

         which is highly effective in adsorbing plant toxins.

      10.5 Elimination

         Forced diuresis, dialysis and haemoperfusion are not helpful 

         in the elimination of cardiac glycosides.

      10.6 Antidote/antitoxin treatment

         10.6.1 Adults

                Digoxin-specific Fab antibody fragments, have been 

                used  successfully in an adult patient intoxicated 

                with Nerium Oleander  (Shamaik, 1988).  The same may 

                apply to Thevetia poisoning.

         10.6.2 Children

                No data available.  (see above)

      10.7 Management discussion

         The use of digoxin specific Fab fragments deserves further 

         evaluation.

 

  1. ILLUSTRATIVE CASES

      11.1 Case reports from literature

         Children: In South West Africa two children were poisoned 

         after eating  the kernel of a seed; one died six hours later 

         (Watt & Breyer-Brandwijk,  1962).

         

         A presumed case of fatal Thevetia poisoning was observed by 

         Ansford & Morris  (1981), in a 3 year-old child who had 

         played near a yellow oleander tree and  was taken to 

         hospital.  The child showed characteristic symptoms and the 

         presence of cardiac  glycoside was detected by radio-

         immunoassay of heart muscle.

         

         Analysis of 170 cases due to yellow Oleander (T. peruviana) 

         seed poisoning  admitted to the Teaching Hospital, Jaffna 

         between January 1983 and December  1985 over a 3-year period 

         showed the following: 

         

         The number of seeds ingested varied from 0.5 – 20 (mean 

         3.5). Patients were  admitted between 15 minutes and 38 

         hours after ingestion (mean 7.2 hours).

         

         The common presenting symptoms were: vomiting (68%), 

         giddiness (36%) and diarrhoea (22%).  Other symptoms 

         included abdominal pain (6%), numbness of mouth and tongue 

         (4.%) and palpitations (3%).  13% of the patients remained  

         asymptomatic.  ECG changes were recognized in 62% of the 

         cases which  included first degree, second degree and 

         variable A-V blocks.

         

         Bradycardia was seen in  50% of the patients.  Only 35% of 

         the cases showed  flattening or inversion of T waves.  ST 

         depression was seen in 24% of the  cases whcih was sometimes 

         deep and “saucer” shaped.  Ventricular and atrial ectopic 

         beats were seen in 7 and 3% of the cases respectively.  

         Seven patients died (Saravanapavananthan & Ganeshmoorthey 

         1986).

      11.2 Internally extracted data on cases

         (In preparation)

      11.3 Internal cases

  1. ADDITIONAL INFORMATION

      12.1 Availability of antidotes/antitoxins

         Fab antibody fragments may be used, if available.

      12.2 Specific preventive measures

      12.3 Other

         The cardiac glycoside peruvoside, from yellow oleander, has 

         been used  medicinally for cardiac insufficiency (Frohne and 

         Pfander, 1983).

         

         It has been found that the  margin between the therapeutic 

         and the toxic  limit is too small for thevetin to prove a 

         useful therapeutic agent (Warr & Breyer-Brandwijk, 1962).

  1. REFERENCES

      13.1 Clinical and toxicological

         Ansford AJ & Morris H (1981).  Fatal Oleander Poisoning. 

         Medical J.  Australia, 1: 360-361.   

 

         

         Arnold HL, Middleton WS, & Chen KK (1935).  The action of 

         Thevetin, a cardiac glycoside and its clinical application.  

         American J. Med. Sci,  189-193.

         

         Duke JA (1987) ed. Handbook of Medicinal Herbs.  USA, CRC 

         Press, Inc.

         

         Ellenhorn MJ & Barceloux DG (1988).  1st ed. Medical 

         Toxicology – Diagnosis  and treatment of Human poisoning, 

         New York, Elsevier Science Publishing  Company Inc. 1252-

         1255.

         

         Frohne D & Pfander HJ (1983).   Ed. A Colour Atlas of 

         Poisonous Plants,  Germany, Wolfe Publishing Ltd., 47.

         

         Lampe KF & McCann MA (1985).  Ed. AMA Handbook of Poisonous 

         and Injurious  Plants, Chicago, Illinois American Medical 

         Association, 169.

         

         Merck Index (1976).  Ed. Windholz M, Merck & Co., USA.

         

         Saravanapavananthan N & Ganeshmoorthy J (1986).  Yellow 

         oleander poisoning – a study of 170 cases.  Proceedings of 

         the 2nd Indo-Pacific Congress on Legal Medicine & Forensic 

         Sciences, 49. (Abstract).

         

         Saravanapavananthan T. (1985).  Plant poisoning in Sri 

         Lanka. Jaffna Medical  Journal, 20(1): 17-21.

         

         Shaw D & Pearn J (1979).  Oleander Poisoning. Medical 

         Journal of Australia,  2: 267-269.

         

         Watt JM & Breyer-Brandwijk MG (1962).   ed. The Medicinal & 

         Poisonous Plants  of Southern & Eastern Africa.  Edinburgh & 

         London, E & S Livingstone Ltd,  107-109.

      13.2 Botanical

  1. AUTHOR(S), REVIEWER(S), DATE(S) (INCLUDING UPDATES), COMPLETE 

    ADDRESS(ES)

    Author:   Dr Ravindra Fernando and Miss Deepthi Widyaratna

              National Poison Information Centre

              General Hospital

              Colombo 8

              Sri Lanka

    

              Tel:

              Fax:

    

    Date:     October 1989

    

    Reviewer: Dr J. Pronczuk

              CIAT 7° piso

              Hospital de Clinicas

              Av. Italia s/n

              Montevideo

              Uruguay

 

    

              Tel: 598-2-470300

              Fax: 598-2-470300

    

    Date:     March 1990

    

    Peer review:   London, March 1990

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